PReD-Bench/PRed-Bench huggingface dataset:
Hepatitis C virus proteins inhibit C3 complement production
Authors: Hangeun Kim
Ratna B Ray
Keith Meyer
Budhaditya Mazumdar
Adrian M Di Bisceglie
Sandip K Bose
Ranjit Ray
Journal: Journal of virology (2012)
Discipline: MICROBIOLOGY
Keywords: complement; C3; hepatitis C virus; HCV; liver biopsy
Affiliations: Departments of Internal Medicine, Saint Louis University, Saint Louis, Missouri, USA.

Abstract:  The third component of human complement (C3) plays a central role in innate immune function as its activation is required to trigger classical as well as alternative complement pathways. In this study, we have observed that sera from patients chronically infected with hepatitis C virus (HCV) displayed significantly lower C3 levels than sera from healthy individuals. Liver biopsy specimens from the same patients also exhibited lower C3 mRNA expression than liver tissues from healthy donors. C3 mRNA level was reduced in hepatocytes upon infection with cell culture-grown HCV genotype 1a or 2a in vitro. Further analysis suggested that HCV core protein displayed a weak repression of C3 promoter activity by downregulating the transcription factor farnesoid X receptor (FXR). On the other hand, HCV NS5A protein strongly downregulated C3 promoter activity at the basal level or in the presence of interleukin-1β (IL-1β) as an inducer. In addition, the expression of the transcription factor CAAT/enhancer binding protein beta (C/EBP-β), which binds to the IL-1/IL-6 response element in the C3 promoter, was inhibited in liver biopsy specimens. Furthermore, expression of C/EBP-β was reduced in hepatocytes infected with cell culture-grown HCV, as well as in hepatocytes transfected with the NS5A genomic region of HCV. Together, these results underscore the role of HCV NS5A protein in impairing innate immune function. 

Retracted: No

PubPeer comments:
 Fig 4F: Appears to be the same panel as Fig 2B from Mazumdar et al. 2013 (doi: [10.1128 jvi.06577-11] ) ![file] , 
 #1 I agree that the bands apparently look similar in these publications of 6-7 years back. Now, it is very difficult to track results from the original experiments. However, results presented from multiple experiments suggested increased CD55 expression, and the concerns raised do not compromise the theme of our publications. Moreover, subsequent follow-up work and publications further emphasized CD55 upregulation by HCV (Fig. 1A - The Journal of Immunology, 1127-1136, 2016). ,
<p>Rapid mineralization of hierarchical poly(l-lactic acid)/poly(ε-caprolactone) nanofibrous scaffolds by electrodeposition for bone regeneration</p>
Authors: YanZhong Zhang
Li Liang
Yiming Gao
Wei Nie
Gregory James Gillispie
ChuangLong He
David James McCoul
Journal: International Journal of Nanomedicine (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: bone repair; electrodeposition; hierarchical porous scaffold; mineralization.
Affiliations: State Key Laboratory for Modification of Chemical Fibers and Polymer Materials, College of Chemistry, Chemical Engineering and Biotechnology, Donghua University, Shanghai 201620, People's Republic of China., Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston Salem, NC 27103, USA., Department of Plastic and Cosmetic Surgery, Shanghai Traditional Chinese Medicine University Affiliated Shuguang Hospital, Shanghai 201203, People's Republic of China., Department of Respiratory Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201999, People's Republic of China.

Abstract:  Introduction: Hierarchical nanofibrous scaffolds are emerging as a promising bone repair material due to their high cell adhesion activity and nutrient permeability. However, the existing method for hierarchical nanofibrous scaffolds fabrication is complicated and not perfectly suitable for further biomedical application in view of both structure and function. In this study, we constructed a hierarchical nanofibrous poly (l-lactic acid)/poly(ε-caprolactone) (PLLA/PCL) scaffold and further evaluated its bone healing ability. Methods: The hierarchical PLLA/PCL nanofibrous scaffold (PLLA/PCL) was prepared by one-pot TIPS and then rapidly mineralized at room temperature by an electrochemical deposition technique. After electrode-positioning at 2 V for 2 hrs, a scaffold coated with hydroxyapatite (M-PLLA/PCL) could be obtained. Results: The pore size of the M-PLLA/PCL scaffold was hierarchically distributed so as to match the biophysical structure for osteoblast growth. The M-PLLA/PCL scaffold showed better cell proliferation and osteogenesis activity compared to the PLLA/PCL scaffold. Further in vivo bone repair studies indicated that the M-PLLA/PCL scaffold could accelerate defect healing in 12 weeks. Conclusion: The results of this study implied that the as-prepared hydroxyapatite coated hierarchical PLLA/PCL nanofibrous scaffolds could be developed as a promising material for efficient bone tissue repair after carefully tuning the TIPS and electrodeposition parameters. 

Retracted: No

PubPeer comments:
 Fig 5A ![file] , 
 I am Wei Nie. The first author of this Paper. Many thanks for pointing out this. By comparing the original file of CT. We found that when processing the data, the different sets of slices were mixed. This makes the data of the same time period wrongly arranged at different points when arranging these pictures. We are in contact with the magazine for errata. ,
BLM helicase facilitates Mus81 endonuclease activity in human cells
Authors: Sagar Sengupta
Curtis C Harris
Clare H McGowan
Steven P Linke
Qin Yang
Ran Zhang
John Bradsher
Nozomu Yanaihara
Veronique Blais
Journal: Cancer Research (2005)
Discipline: CLINICAL MEDICINE
Keywords: Bloom syndrome; BLM; RecQ helicase; replication; recombination
Affiliations: Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892-4255, USA.

Abstract:  Bloom syndrome is a rare, autosomal recessive inherited disorder in humans. The product of the Bloom syndrome mutated gene, designated BLM, is a member of the RecQ helicase family. BLM has been proposed to function at the interface of replication and recombination, and to facilitate the repair of DNA damage. Here, we report in vivo physical interaction and colocalization of BLM and a DNA structure-specific endonuclease, Mus81, at sites of stalled replication forks outside the promyelocytic leukemia nuclear bodies during the S-phase arrest of the cell cycle. Amino acids 125 to 244 of Mus81 interact with the C-terminal region (amino acids 1,007-1,417) of BLM. Whereas Mus81 does not have any effect on the helicase activity of BLM, BLM can stimulate Mus81 endonuclease activity on the nicked Holliday junctions and 3' flap. This stimulation is due to enhanced binding of Mus81 to the DNA substrates. These data suggest a new function of BLM in cooperating with Mus81 during processing and restoration of stalled replication forks. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than expected. ![file] , 
 Figure 4A. Much more similar than expected. ![file] ,
MicroRNA‑10b suppresses the migration and invasion of chondrosarcoma cells by targeting brain‑derived neurotrophic factor
Authors: Abudunaibi Aili
Yong Chen
Hongqi Zhang
Journal: Molecular Medicine Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; mRNA degradation; protein translation; 3'‑untranslational region; miR‑10b
Affiliations: Department of Spinal Surgery, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  MicroRNAs (miRs) can lead to mRNA degradation or inhibit protein translation through directly binding to the 3'‑untranslational region (UTR) of their target mRNAs. Deregulation of miR‑10b has been reported to be associated with chondrosarcoma. However, the role of miR‑10b in chondrosarcoma cell migration and invasion, as well as the underlying mechanisms, has not been investigated. In the present study, it was demonstrated that miR‑10b was notably downregulated in the JJ012 and SW1353 chondrosarcoma cell lines compared with the TC28a2 normal chondrocyte line. Treatment with DNA demethylating agent 5‑aza‑2'‑deoxycytidine and histone deacetylase inhibitor 4‑phenylbutyric acid, or transfection with miR‑10b mimics promoted the expression of miR‑10b, which further suppressed the migratory and invasive capacities of JJ012 chondrosarcoma cells. Moreover, brain‑derived neurotrophic factor (BDNF) was identified as a novel target of miR‑10b, and its protein expression level was negatively regulated by miR‑10b in JJ012 cells. Furthermore, overexpression of BDNF reversed the inhibitory effect of miR‑10b upregulation on the migration and invasion of JJ012 cells. In addition, the data suggest that matrix metalloproteinase 1 (MMP1) may be involved in the miR‑10b/BDNF‑mediated chondrosarcoma cell migration and invasion in JJ012 cells. In conclusion, these findings suggest that miR‑10b/BDNF may serve as a potential therapeutic target for chondrosarcoma. 

Retracted: Yes

PubPeer comments:
 Figure 2B. Much more similar than you would expect. ![file] , 
 ![file] ,
Inhibition of cyclooxygenase-2 suppresses invasiveness of oral squamous cell carcinoma cell lines via down-regulation of matrix metalloproteinase-2 and CD44
Authors: Masao Nagumo
Hidetoshi Ito
Yuji Kurihara
Yuriko Kinugasa
Masashi Hatori
Daisuke Ito
Journal: Clinical & Experimental Metastasis (2005)
Discipline: CLINICAL MEDICINE
Keywords: COX-2; angiogenesis; immunity suppression; tumor invasion; oral squamous cell carcinoma
Affiliations: Second Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University, Tokyo, Japan.

Abstract:  Expression of cyclooxygenase-2 (COX-2) in tumors is known to be associated with enhanced angiogenesis, suppression of host immunity, and tumor invasion. In the present study, human oral squamous cell carcinoma (OSCC) cell lines NA and HSC-4 were used to evaluate the effects of NS-398, a selective inhibitor of COX-2, and COX-2 antisense oligonucleotide (COX-2 AS) on the invasion activity of OSCC cells. Matrigel invasion assay revealed that the invasiveness of NA and HSC-4 was suppressed by treatment with either NS-398 or COX-2 AS. These reagents down-regulated the secretion of matrix metalloproteinase-2 (MMP-2) to culture supernatant as well as the expression of MMP-2 mRNA and protein. Membrane-type 1 matrix metalloproteinase (MT1-MMP), an activator of proMMP-2, was also down-regulated by treatment with these reagents. Furthermore, expression of CD44 on the surface of these cells was reduced by treatment with either NS-398 or COX-2 AS. In addition, MMP-2 antisense oligonucleotides reduced the expression of CD44 on the surface of both OSCC cell lines. These findings suggest that NS-398 and COX-2 AS suppress the invasiveness of OSCC cells via down-regulation of MMP-2 and CD44. Genetic or pharmacological inhibition of COX-2 may therefore be a beneficial strategy in the treatment of OSCC patients. 

Retracted: No

PubPeer comments:
 Figure 4, GAPDH controls for RT-PCR analysis of MMP-2 on different cell lines (NA and HSC-4) look more similar than expected (red boxes). Although this article is 17-year-old, could the authors please check? ![file] ,
Requirement for pre-existing of p21 to prevent doxorubicin-induced apoptosis through inhibition of caspase-3 activation
Authors: C Shen
Y J Lu
J J Tang
Journal: Molecular and Cellular Biochemistry (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Doxorubicin; apoptosis; p21; CDK inhibitor; colorectal cancer
Affiliations: Cancer Research Center, Celstar Bio-Pharmaceutical Co. Ltd., Shanghai, PR China.

Abstract:  Doxorubicin (DOX)-induced apoptosis is suppressed by p21 (waf1/cip1/sdi1), a cyclin dependent kinase (CDK) inhibitor. Here we show that exogenous expression of p21 before, but not after, the DOX-treatment protected p21-deficient human colorectal cancer cell line DLD1 from DOX-induced apoptosis. In previous work, we demonstrated that p21 inhibits DOX-induced apoptosis via its CDK-binding and CDK-inhibitory activity. Here we report that pre-existing p21 can associate with pro-caspase-3 and inhibit caspase-3 activation in the cells, which was at least in part responsible for enhancing survival of DOX-treated cells. Furthermore, the N-terminal domain of p21 was found to interact with pro-caspase-3 in DLD1 cells. Thus, we propose that pre-existing p21 is required to prevent DOX-induced apoptosis. 

Retracted: No

PubPeer comments:
 Fig 2D:  Euxanthone suppressed D. migratory capacity ... of CRC cells. ![file] Annotated to show panels shared with 2A of [Zhang et al (2020)] and 6J K of [Yin et al (2020)] . ![file] , 
 Fig 2A,  Euxanthone promotes apoptosis, as shown by A. TUNEL assay . Below: Fig 2B from [Zhu et al (2018)] ,  Euxanthone promotes apoptosis in SKOV3 and OVCAR3 cells..... B. Cells were treated with euxanthone for 48 h and apoptosis was assessed by TUNEL assay. ![file] If you are like me you are wondering how these two IHC fluorescence images can find their way into two papers by unconnected authors, but vertically flipped, and attached to different cell types. , 
 Fig 2E,  invasiveness .. of CRC cells. ![file] At right, for comparison, Fig 2(e) of [Zhang et al (2020)] ,  The cell invasion was measured by transwell assay . The Control panels also appear in Fig 2E of [Liu et al (2018)] . , 
 ![file] ![] ,
JAGGED1 gene expression during human embryogenesis elucidates the wide phenotypic spectrum of Alagille syndrome
Authors: T Attié-Bitach
M Meunier-Rotival
M Vekemans
S Audollent
F Encha-Razavi
M Hadchouel
C Crosnier
F Soudy
Journal: Hepatology (2000)
Discipline: CLINICAL MEDICINE
Keywords: JAGGED1 gene; NOTCH receptor ligand; Alagille syndrome; human embryogenesis; in situ hybridization
Affiliations: Unité INSERM 347 affiliée au CNRS, Le Kremlin-Bicêtre Cedex, France.

Abstract:  Mutations of the JAGGED1 gene, encoding a NOTCH receptor ligand, cause Alagille syndrome (AGS), a complex malformative disorder affecting mainly the liver, heart, vertebrae, eye, and face. Minor and occasional features involving kidney, pharynx, systemic arteries, skeleton, and ear are in some cases associated with the syndrome. To describe the expression of JAGGED1 during human embryogenesis and to study its relationship with all the features of AGS, we performed in situ hybridization studies on human embryos and fetal tissue sections. JAGGED1 was mainly expressed in the cardiovascular system. In the liver, JAGGED1 transcripts were only detected in blood vessels. JAGGED1 was also expressed in other structures of mesenchymal origin (distal mesenchyme of limb buds; mesonephric and metanephric tubules of the kidney) and in epithelial structures including the ciliary margin of the retina and the posterior part of the lens, the ventral epithelium of the otic vesicle, the neurosensory epithelium of the ear vestibule, the epithelium of pharyngeal arches, and the developing central nervous system. The strong JAGGED1 expression during human embryo- and feto-genesis both in the vascular system and in other mesenchymal and epithelial tissues implicates abnormal angiogenesis in the pathogenesis of Alagille syndrome and particularly the paucity of interlobular bile ducts. However, it is probably not the only mechanism of the disease. Except for the central nervous system, there is a strong correlation between JAGGED1 expression and all the features of AGS. This implies that the features occasionally associated with the syndrome are not coincidental. 

Retracted: No

PubPeer comments:
 ![file] According to the authors, vessels indicated by p are supposed to be pulmonary arteries. These structures are located dorsally to the coelomic cavity in the peritracheal mesenchyme. This is not the anatomical location of the pulmonary arteries. These vessels are supra-aortic trunks. ,
Principles of cellular resource allocation revealed by condition-dependent proteome profiling
Authors: Naama Barkai
Ilya Soifer
Moshe Kafri
Yonat Gurvich
Eyal Metzl-Raz
Gilad Yaakov
Journal: eLife (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: S. cerevisiae; cell biology; computational biology; proteome; resource allocation
Affiliations: Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

Abstract:  Growing cells coordinate protein translation with metabolic rates. Central to this coordination is ribosome production. Ribosomes drive cell growth, but translation of ribosomal proteins competes with production of non-ribosomal proteins. Theory shows that cell growth is maximized when all expressed ribosomes are constantly translating. To examine whether budding yeast function at this limit of full ribosomal usage, we profiled the proteomes of cells growing in different environments. We find that cells produce excess ribosomal proteins, amounting to a constant ≈8% of the proteome. Accordingly, ≈25% of ribosomal proteins expressed in rapidly growing cells does not contribute to translation. Further, this fraction increases as growth rate decreases and these excess ribosomal proteins are employed when translation demands unexpectedly increase. We suggest that steadily growing cells prepare for conditions that demand increased translation by producing excess ribosomes, at the expense of lower steady-state growth rate. 

Retracted: No

PubPeer comments:
 A quote from the Discussion:  This question was extensively studied in theoretical models and experimentally in bacteria (Brauer et al., 2008; Bremer and Ehrenberg, 1995; Nomura et al., 1984; Schaechter et al., 1958; Scott et al., 2010; Waldron and Lacroute, 1975; Warner, 1999; Zaslaver et al., 2009), but received relatively little attention in eukaryotic models. Actually, at least three of the cited papers are about growth-rate dependent rRNA and mRNA expression in yeast, not in bacteria (Waldron and Lacroute, 1975, Warner 1999, Brauer et al. 2008) and even have  yeast in their title. The latter reference is from the Botstein group which has published several papers on this topic, incl. a model that can predict growth rate from differential expression of  signature genes. The authors failed to discuss these previous results from yeast. ,
MiR-513a-3p inhibits EMT mediated by HOXB7 and promotes sensitivity to cisplatin in ovarian cancer cells
Authors: D-D Zhang
Y Zhao
Y Chen
X-H Zhao
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-513a-3p; ovarian cancer cells; biological function; mechanism of action; qRT-PCR
Affiliations: Department of Gynecology and Obstetrics, Ningbo Zhenhai Lianhua Hospital, Ningbo, China. .

Abstract:  Objective: Our aim was to investigate the biological function and mechanism of action of miR-513a-3p in ovarian cancer cells. Materials and methods: In this study, qRT-PCR, Western blots, and immunohistochemistry experiments were among the methods used to examine the expression of miR-513a-3p, HOXB7, and related transcripts within ovarian cancer cells. An MTT assay was conducted to evaluate the viability of ovarian cancer cells in the presence of cisplatin. Transwell and wound-healing assays were performed to examine cell migration and invasion. Dual-Luciferase reporter assays were used to evaluate interactions among the aforementioned target genes. In vivo tumorigenesis experiments were conducted to verify biological effects of miR-513a-3p and HOXB7. Results: HOXB7 expression was relatively higher and MiR-513a-3p expression was relatively lower in ovarian cancer cells. Down-regulated expression of miR-513a-3p promoted cell movement via its ability to regulate epithelial-mesenchymal transition (EMT). Furthermore, decreased expression of miR-513a-3p resulted in increased sensitivity to cisplatin and resulted in poor prognosis in ovarian cancer patients who had relapsed after treatment with cisplatin. However, HOXB7 reversed the impact of miR-513a-3p in ovarian cancer cells. These results suggested that miR-513a-3p altered EMT mediated by HOXB7 and cisplatin-resistance. Conclusions: MiR-513a-3p plays a critical role in promoting sensitivity to cisplatin and tumorigenesis via targeting HOXB7 in ovarian cancer. 

Retracted: No

PubPeer comments:
 Figure 2C and 2D show data obtained from ovarian cancer patients. However, there is nothing in the Methods about where and how these samples were obtained, if patients gave informed consent, or if IRB approval was obtained and by which of the two hospitals (Ningbo Zhenhai Lianhua Hospital or Maternal and Child Health Hospital of Zibo City). ![file] , 
 Figs 2D, 4G.  Kaplan-Meier analysis was performed to determine the relationship between miR-513a-3p expression and survival rates among patients who relapsed after cisplatin treatment for ovarian cancer ...  Kaplan-Meier analysis of the survival rates of ovarian cancer patients who relapsed after cisplatin chemotherapy . The two pairs of curves are not compatible. They cannot be derived from a single set of survival times by dichotomising the patients according to different criteria. In particular, from 50 months on, **both** 4G curves show higher survival than their 2D counterparts. ![file] ,
MicroRNA-495 confers inhibitory effects on cancer stem cells in oral squamous cell carcinoma through the HOXC6-mediated TGF-β signaling pathway
Authors: Zhengyu Zhou
Wenzheng Luo
Wen Chen
Heqiang Zhou
Xiaolong You
Xiaoyong Wei
Journal: Stem Cell Research & Therapy (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cancer stem cells; Epithelial-mesenchymal transition; Homeobox C6; Invasion; Migration
Affiliations: Department of Head and Neck Surgery, Jiangxi Cancer Hospital, No. 519, Beijing East Road, Nanchang, 330029, Jiangxi Province, People's Republic of China., Department of Intensive Care Medicine, Jiangxi Cancer Hospital, Nanchang, 330029, People's Republic of China., Department of Plastic Surgery, Jiangxi Cancer Hospital, Nanchang, 330029, People's Republic of China., Department of Liver Oncology, Jiangxi Cancer Hospital, Nanchang, 330029, People's Republic of China., Department of Head and Neck Surgery, Jiangxi Cancer Hospital, No. 519, Beijing East Road, Nanchang, 330029, Jiangxi Province, People's Republic of China. .

Abstract:  Background: Oral squamous cell carcinoma (OSCC) is associated with high morbidity and ranks sixth among malignancies worldwide. Increasing evidence suggests that microRNAs (miRNAs or miRs) play a critical role in regulating cancer stem cells (CSCs), which drive the proliferation and spread of OSCC. Therefore, based on the alteration of aberrantly expressed miR-495 and homeobox C6 (HOXC6) by Gene Expression Omnibus (GEO) analysis, we subsequently explore the potential effect of miR-495 on the progression of CSCs in OSCC. Methods: After the isolation of CSCs from the clinical tissue samples of OSCC patients, the expression of miR-495 and HOXC6 was determined, followed by the validation of the relationship between miR-495 and HOXC6. Subsequently, gain- and loss-function approach was performed to detect the role of miR-495 and HOXC6 in cell proliferation, migration, invasion, cell cycle entry, apoptosis, and epithelial-mesenchymal transition (EMT) of CSCs in OSCC, as well as the tumor growth in vivo. Results: HOXC6 was highly expressed while miR-495 was poorly expressed in OSCC. HOXC6 was verified to be a target gene of miR-495, and miR-495 could inhibit the activation of the TGF-β signaling pathway. CSCs with miR-495 overexpression or HOXC6 silencing exhibited reversed EMT process; reduced abilities of proliferation, migration, and invasion; and promoted cell apoptosis in vitro. Moreover, inhibited tumor growth was observed in vivo after injection with miR-495 agomir or sh-HOXC6. In contrast, the downregulation of miR-495 showed an induced role in the progression of OSCC. Conclusion: These findings suggest that miR-495 may suppress HOXC6 to inhibit EMT, proliferation, migration, and invasion while promoting apoptosis of CSCs in OSCC by inhibiting the TGF-β signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 4 appears to have image duplications ![file] , 
 Fig 5a,b.  Cell cycle entry after different treatments examined by PI staining . ![file] These flow-cytometry cell-cycle plots appear to be hand-drawn. Overhangs. Arbitrary, irregular S profiles. Lines that simply don t add up. ,
IFN-γ induces upregulation of TNF-α, downregulation of MMP-2 and MMP-9 expressions in abortion rat
Authors: Q Sun
Y He
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: TNF-α; MMP-2; MMP-9; IFN-γ; abortion
Affiliations: Department of Obstetrics, Jinan Maternity and Child Care Hospital, Jinan, Shandong, China. .

Abstract:  Objective: Tumor necrosis factor-α (TNF-α) participates in the regulation of the whole process of pregnancy. Matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) play important roles in the process of trophoblast invading decidua. This research aims to determine the role of IFN-γ in TNF-α, MMP-2, and MMP-9 of abortion rats. Materials and methods: The rats were divided into control, abortion model, gestation, and IFN-γ group. Abortion rats model in IFN-γ group were treated by IFN-γ at low and high doses upon abortion model. Serum and tissue TNF-α, MMP-2, and MMP-9 expressions were detected by ELISA and immunohistochemistry. Results: The level of TNF-α was significantly elevated, while MMP-2 and MMP-9 were statistically declined in the serum and decidual tissue of rat from model group (p &lt; 0.05). Of note, the expression of TNF-α was further increased, whereas MMP-2 and MMP-9 reduced in IFN-γ high dose group (p &lt; 0.05). Conclusions: We demonstrated that in abortion rats, TNF-α was overexpressed, while MMP-2 and MMP-9 were reduced declined in the serum and decidual tissue. The treatment with a high dose of IFN-γ further upregulated TNF-α expression and decreased MMP-2 and MMP-9 levels, aggravating the severity of rat abortion. 

Retracted: No

PubPeer comments:
 The 15 panels of Figs 1-3 are all marked by curious repeated glitches in their lower-right corners, with sharp-edged, curved discontinuities. ![file] Especially distinct in 2G, 3O. ![file] ,
MiR-101 promotes nasopharyngeal carcinoma cell apoptosis through inhibiting Ras/Raf/MEK/ERK signaling pathway
Authors: J-J Zhu
H-L Lin
R-S Wu
E-H Qiu
J-R Wang
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: ERK/MAPK signaling pathway; miR-101; MEK1; NPC pathogenesis; cell proliferation
Affiliations: Department of Otolaryngology, the 2nd Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China. .

Abstract:  Objective: Extra-cellular signal regulated kinase (ERK)/mitogen activated protein kinase (MAPK) signaling pathway is widely involved in cell proliferation and apoptosis. MAPK kinase 1 (MEK1) is the upstream protein kinase of ERK that can activate ERK/MAPK signaling pathway. microRNA-101 (MiR-101) down-regulation is found to be associated with nasopharyngeal carcinoma (NPC) pathogenesis. Bioinformatics analysis shows the complementary targeted relationship between miR-101 and the 3'-UTR of MEK1 mRNA. This study explores the role of miR-101 in regulating MEK1 expression, ERK/MAPK signaling pathway activation, and NPC pathogenesis. Materials and methods: Dual luciferase assay confirmed the targeted relationship between miR-101 and MEK1. MiR-101 and MEK1 expressions were compared in inflammatory nasopharynx tissue and NPC tissue. MiR-101, MEK1, phosphorylated ERK 1/2 (p-ERK1/2), survivin expressions in NP69, CNE-1, HONE1, and C666-2 cell lines were detected. NPC cell line C666-1 was cultured in vitro and divided into four groups, including miR-NC, miR-101, si-NC and si-MEK1. Cell apoptosis was determined by flow cytometry. Cell proliferation was evaluated by EdU staining. Results: MiR-101 targeted inhibited MEK1 expression. MiR-101 was significantly down-regulated, while MEK1 was significantly elevated in NPC tissue compared with inflammatory nasopharynx tissue. MiR-101 was markedly declined, whereas MEK1, p-ERK1/2, and survivin were apparently increased in CNE-1, HONE1, and C666-1 cells compared with NP69 cells. MiR-101 mimic and/or si-MEK1 transfection significantly reduced MEK1, p-ERK1/2, and survivin levels, attenuated cell proliferation, and enhanced cell apoptosis. Conclusions: Down-regulation of miR-101 was related to NPC pathogenesis. MiR-101 elevation suppressed NPC cell proliferation and promoted apoptosis through targeted inhibiting MEK1 expression to alleviate ERK/MAPK signaling pathway and survivin expression. 

Retracted: Yes

PubPeer comments:
 The article u201cMiR-101 promotes nasopharyngeal carcinoma cell apoptosis through inhibiting Ras Raf MEK ERK signaling pathway, by R.-S. Wu, E.-H. Qiu, J.-J. Zhu, J.-R. Wang, H.-L. Lin, published in Eur Rev Med Pharmacol Sci 2018; 22(1): 150-157u2013DOI: 10.26355 eurrev_201801_14112u2013PMID: 29364482u201d has been withdrawn from the authors. [The Publisher apologizes for any inconvenience this may cause] . ![file] The paper had been flagged in a Google document as showing [the signs of a papermill provenance] . https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit#gid=0 ,
Regulation of Pax3 by proteasomal degradation of monoubiquitinated protein in skeletal muscle progenitors
Authors: Kevin Iori
Stéphane C Boutet
Lauren S Chan
Marie-Hélène Disatnik
Thomas A Rando
Journal: Cell (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Pax3; Pax7; myogenesis; ubiquitination; proteasomal degradation
Affiliations: Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

Abstract:  Pax3 and Pax7 play distinct but overlapping roles in developmental and postnatal myogenesis. The mechanisms involved in the differential regulation of these highly homologous proteins are unknown. We present evidence that Pax3, but not Pax7, is regulated by ubiquitination and proteasomal degradation during adult muscle stem cell activation. Intriguingly, only monoubiquitinated forms of Pax3 could be detected. Mutation of two specific lysine residues in the C-terminal region of Pax3 reduced the extent of its monoubiquitination and susceptibility to proteasomal degradation, whereas introduction of a key lysine into the C-terminal region of Pax7 rendered that protein susceptible to monoubiquitination and proteasomal degradation. Monoubiquitinated Pax3 was shuttled to the intrinsic proteasomal protein S5a by interacting specifically with the ubiquitin-binding protein Rad23B. Functionally, sustained expression of Pax3 proteins inhibited myogenic differentiation, demonstrating that Pax3 degradation is an essential step for the progression of the myogenic program. These results reveal an important mechanism of Pax3 regulation in muscle progenitors and an unrecognized role of protein monoubiquitination in mediating proteasomal degradation. 

Retracted: No

PubPeer comments:
 Fig. 3a: Compare Kidney RA16 with Kidney RNA Library after gradation adjustment. ![file] , 
 Thank you for your careful and critical examination for our article. Actually, weu2019ve explained this query to the journal editors around August of 2018. For the experimental results described in Fig. 3A, serial sections were prepared from the same tissue part and then stained with fluorescently-labeled RA16 or RNA library. Therefore, similar stained view from close sections is possible. The result demonstrated in Fig. 3A is the kidney tissue section as one of the negative tissues (negative control). Conclusive findings described in the article is correct and consistent. We appreciated your admirable scientific spirits. ,
Endoplasmic reticulum localized Bcl-2 prevents apoptosis when redistribution of cytochrome c is a late event
Authors: B Leber
M G Annis
G Kroemer
D W Andrews
L Z Penn
W Zhu
N Zamzami
Journal: Oncogene (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mitochondrial function; Apoptosis; Bcl-2; Endoplasmic reticulum; Cytochrome c
Affiliations: Department of Biochemistry, McMaster University, Hamilton, L8N 3Z5, Canada.

Abstract:  The disruption of mitochondrial function is a key component of apoptosis in most cell types. Localization of Bcl-2 to the outer mitochondrial and endoplasmic reticulum membranes is consistent with a role in the inhibition of many forms of apoptosis. In Rat-1 cells, a Bcl-2 mutant targeted exclusively to the endoplasmic reticulum (Bcl-cb5) was effective at inhibiting apoptosis induced by serum starvation/myc, or ceramide but not apoptosis induced by etoposide. The former conditions cause a decrease in mitochondrial transmembrane potential (Deltapsi(m)) as an early event that precedes the release of cytochrome c from mitochondria. By contrast, when cells are exposed to etoposide, a situation in which cytochrome c release and membrane localization of the pro-apoptotic protein Bax precede loss of Deltapsi(m), wild type Bcl-2 but not Bcl-cb5 prevents apoptosis. Therefore, Bcl-2 functions in spatially distinct pathways of apoptosis distinguished by the order of cytochrome c release and loss of Deltapsi(m). 

Retracted: No

PubPeer comments:
 Fig. 1A u2013 more similar than expected. Could authors check it please? ![file] ,
Absence of erythroblast macrophage protein (Emp) leads to failure of erythroblast nuclear extrusion
Authors: Shashi Bala
Shivani Soni
Luanne L Peters
Kenneth E Sahr
Manjit Hanspal
Babette Gwynn
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: erythroblastic island; Emp; erythropoiesis; enucleation; hematopoiesis
Affiliations: Department of Medicine, Center for Cell Biology, Caritas St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA.

Abstract:  In mammals, the functional unit for definitive erythropoiesis is the erythroblastic island, a multicellular structure composed of a central macrophage surrounded by developing erythroblasts. Erythroblast-macrophage interactions play a central role in the terminal maturation of erythroblasts, including enucleation. One possible mediator of this cell-cell interaction is the protein Emp (erythroblast macrophage protein). We used targeted gene inactivation to define the function of Emp during hematopoiesis. Emp null embryos die perinatally and show profound alterations in the hematopoietic system. A dramatic increase in the number of nucleated, immature erythrocytes is seen in the peripheral blood of Emp null fetuses. In the fetal liver virtually no erythroblastic islands are observed, and the number of F4/80-positive macrophages is substantially reduced. Those present lack cytoplasmic projections and are unable to interact with erythroblasts. Interestingly, wild type macrophages can bind Emp-deficient erythroblasts, but these erythroblasts do not extrude their nuclei, suggesting that Emp impacts enucleation in a cell autonomous fashion. Previous studies have implicated the actin cytoskeleton and its reorganization in both erythroblast enucleation as well as in macrophage development. We demonstrate that Emp associates with F-actin and that this interaction is important in the normal distribution of F-actin in both erythroblasts and macrophages. Thus, Emp appears to be required for erythroblast enucleation and in the development of the mature macrophages. The availability of an Emp null model provides a unique experimental system to study the enucleation process and to evaluate the function of macrophages in definitive erythropoiesis. 

Retracted: No

PubPeer comments:
 The bands in Figure 3A were very similar in red boxes. ![file] ,
Electrospun poly(L-lactide)/poly(ε-caprolactone) blend nanofibrous scaffold: characterization and biocompatibility with human adipose-derived stem cells
Authors: Ejun Peng
Yuxi Wang
Xiaolin Xie
Bolin Wu
Liang Chen
Xiaoyong Zeng
Yi Bai
Guiying Liao
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: tissue engineering; polymer; electrospun; PLLA; PCL
Affiliations: Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Abstract:  The essence of tissue engineering is the fabrication of autologous cells or induced stem cells in naturally derived or synthetic scaffolds to form specific tissues. Polymer is thought as an appealing source of cell-seeded scaffold owing to the diversity of its physicochemical property and can be electrospun into nano-size to mimic natural structure. Poly (L-lactic acid) (PLLA) and poly (ε-caprolactone) (PCL) are both excellent aliphatic polyester with almost "opposite" characteristics. The controlling combination of PLLA and PCL provides varying properties and makes diverse applications. Compared with the copolymers of the same components, PLLA/PCL blend demonstrates its potential in regenerative medicine as a simple, efficient and scalable alternative. In this study, we electrospun PLLA/PCL blends of different weight ratios into nanofibrous scaffolds (NFS) and their properties were detected including morphology, porosity, degradation, ATR-FTIR analysis, stress-stain assay, and inflammatory reaction. To explore the biocompatibility of the NFS we synthesized, human adipose-derived stem cells (hASCs) were used to evaluate proliferation, attachment, viability and multi-lineage differentiation. In conclusion, the electrospun PLLA/PCL blend nanofibrous scaffold with the indicated weight ratios all supported hASCs well. However, the NFS of 1/1 weight ratio showed better properties and cellular responses in all assessments, implying it a biocompatible scaffold for tissue engineering. 

Retracted: No

PubPeer comments:
 Concern about Figure 10, communicated with the journal in October 2015. * Green boxes: Left and right Collagen II panels appear to show an overlap, if one of the panels is rotated 180 degrees * Pink boxes: Center and right Collagen II panels appear to show an overlap That means that all three Collagen II panels might be derived from the same specimen. ![file] , 
 Also, Figure 10 s bottom right panel (Oil red  O ) appears to be the same as used in Figure 12 of Gui-Ying Liao et al. Journal of Applied Polymer Science, Vol. 120, 2154u20132165 (2011), DOI: 10.1002 app.33398 ![file] And Figure 1 from this paper appears the same as Figure 1 from Liao et al. Shown here with blue boxes. ![file] ,
Harnessing Colon Chip Technology to Identify Commensal Bacteria That Promote Host Tolerance to Infection
Authors: Diogo M Camacho
Mark J Cartwright
Dennis L Kasper
Michael Super
Donald E Ingber
Matheus F Silva Palazzo
Francis N Grafton
Francesca S Gazzaniga
Alexandre L M Dinis
Meng Wu
Journal: Frontiers in Cellular and Infection Microbiology (2021)
Discipline: MICROBIOLOGY
Keywords: gut; infection; intestine; microbiome; microfluidic
Affiliations: Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, MA, United States., Department of Immunology, Harvard Medical School, Boston, MA, United States., Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil., Vascular Biology Program and Department of Surgery, Boston Children's Hospital and Harvard Medical School, Boston, MA, United States., Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, United States.

Abstract:  Commensal bacteria within the gut microbiome contribute to development of host tolerance to infection, however, identifying specific microbes responsible for this response is difficult. Here we describe methods for developing microfluidic organ-on-a-chip models of small and large intestine lined with epithelial cells isolated from duodenal, jejunal, ileal, or colon organoids derived from wild type or transgenic mice. To focus on host-microbiome interactions, we carried out studies with the mouse Colon Chip and demonstrated that it can support co-culture with living gut microbiome and enable assessment of effects on epithelial adhesion, tight junctions, barrier function, mucus production, and cytokine release. Moreover, infection of the Colon Chips with the pathogenic bacterium, Salmonella typhimurium, resulted in epithelial detachment, decreased tight junction staining, and increased release of chemokines (CXCL1, CXCL2, and CCL20) that closely mimicked changes previously seen in mice. Symbiosis between microbiome bacteria and the intestinal epithelium was also recapitulated by populating Colon Chips with complex living mouse or human microbiome. By taking advantage of differences in the composition between complex microbiome samples cultured on each chip using 16s sequencing, we were able to identify Enterococcus faecium as a positive contributor to host tolerance, confirming past findings obtained in mouse experiments. Thus, mouse Intestine Chips may represent new experimental in vitro platforms for identifying particular bacterial strains that modulate host response to pathogens, as well as for investigating the cellular and molecular basis of host-microbe interactions. 

Retracted: No

PubPeer comments:
 One of the reviewer is a lab alumni of the last author s lab and has co-authored paper on the same topic in 2019. Is that counted as conflict of interest? ,
MicroRNA-195 inhibits the behavior of cervical cancer tumors by directly targeting HDGF
Authors: Rongrong Song
Guantai Ni
Yunxia Sun
Min Chen
Honmei Sun
Lin Cong
Meiling Chen
Journal: Oncology letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: cervical cancer; hepatoma-derived growth factor; metastasis; microRNA-195.
Affiliations: Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China., Prenatal Diagnosis Center, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China., Department of Obstetrics and Gynecology, The People's Hospital of Xuancheng, Xuancheng, Anhui 242000, P.R. China., Department of Obstetrics and Gynecology, The First Affiliated Hospital of Wannan Medical College, Wuhu, Anhui 241001, P.R. China.

Abstract:  MicroRNAs (miRNAs/miRs) are a class of conserved non-coding endogenous small regulatory RNAs that regulate target gene expression by binding to the 3'-untranslated region of target mRNAs in a base-pairing manner, resulting in repression of transcription or degradation of target mRNAs. It has been demonstrated previously that the abnormal expression of miRNAs is involved in the carcinogenesis and progression of cervical cancer. The aim of the present study was to investigate the expression, biological functions and underlying molecular mechanisms of miR-195 in cervical cancer. The reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression level of miR-195 in cervical cancer tissues and cell lines. Following transfection, an MTT assay, cell migration and invasion assays, western blot analysis and a dual-luciferase reporter assay were performed in human cervical cancer cells. In the present study, it was identified that miR-195 was downregulated in cervical cancer tissues and cell lines. Additionally, upregulation of miR-195 and knockdown of hepatoma-derived growth factor (HDGF) inhibited proliferation, migration and invasion of cervical cancer cells. Furthermore, a dual-luciferase reporter assay identified that HDGF was a direct target gene of miR-195. RT-qPCR and western blot analysis demonstrated that miR-195 mimic inhibited HDGF expression at the mRNA and protein levels, whereas miR-195 inhibitor enhanced HDGF expression at the mRNA and protein levels. These results indicated that miR-195 targeted HDGF to inhibit the behavior of tumors in cervical cancer. These results also suggested that miR-195 was a potential therapeutic biomarker of cervical cancer. 

Retracted: No

PubPeer comments:
 Image concerns in this paper were found during a systematic search of papers in Spandidos journals for possible duplicated images. Figure 5C. * Red and pink boxes: Three of the HDGF siRNA panels representing different experiments (different cell lines and migration vs invasion) appear to shown areas of overlap. ![file] ,
Long noncoding RNA NORAD promotes the progression of retinoblastoma by sponging miR 136-5p/PBX3 axis
Authors: Y-J Hao
B Wang
X-L Yang
X-L Gu
X-X Wang
J-F Sun
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Long noncoding RNA; NORAD; retinoblastoma; miR-136-5p; PBX3 axis
Affiliations: Department of Ophthalmology, Qilu Hospital of Shandong University, Jinan, Shandong Province, China.

Abstract:  The article "Long noncoding RNA NORAD promotes the progression of retinoblastoma by sponging miR-136-5p/PBX3 axis, by X.-L. Yang, Y.-J. Hao, B. Wang, X.-L. Gu, X.-X. Wang, J.-F. Sun, published in Eur Rev Med Pharmacol Sci 2020; 24(3):1278-1287. DOI: 10.26355/eurrev_202001_20185. PMID: 32096159" has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. 

Retracted: No

PubPeer comments:
 According to the publisher s website, this paper  has been withdrawn from the authors.  The Publisher apologizes for any inconvenience this may cause. At the time of writing, the paper was still available through the internal link, https: www.europeanreview.org wp wp-content uploads 1278-1287.pdf. I have a question about Fig 4(F,G):  F, MiR136-5p was negatively correlated with PBX3 in RB tissues. G, PBX3 was negatively correlated with NORAD in RB tissues. The 24 values of PBX3 range from about 0.3 to 2.1 in 4F (where they re the vertical axis), and from about 0.1 to 1.4 in 4G (horizontal axis). ![file] It occurred to me that perhaps the scales are mislabeled in 4G, and PBX3 is really on the *vertical* axis, but that doesn t work either. ,
IGHG1 functions as an oncogene in tongue squamous cell carcinoma via JAK1/STAT5 signaling
Authors: H-Q Ma
Y-L Zheng
Y-Y Li
J-F Xie
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: IGHG1; tongue squamous cell carcinoma; progression; mechanisms; expression patterns
Affiliations: Department of Stomatology, Jining No. 1 People's Hospital, Jining, Shandong, China. .

Abstract:  Objective: We explored the IgG1 heavy chain constant region (IGHG1) roles in tongue squamous cell carcinoma (TSCC) progression, as well as to probe the underlying mechanisms. Patients and methods: The expression patterns of IGHG1 in TSCC tissues and cell lines were tested by Western blotting, quantitative real-time PCR (RT-PCR) and immunohistochemistry (IHC) technologies. The relationship between IGHG1 expression level and the overall survival and clinicopathologic features of patients with TSCC were evaluated to assess the clinical value of IGHG1. The effects of IGHG1 on cell function were determined by Cell-Counting Kit-8 (CCK-8), clone formation, flow cytometry and in vivo tumor formation assays. Results: The expression of IGHG1 in TSCC tissues and cell lines was significantly elevated at both mRNA and protein levels. IGHG1 expression levels closely related to T classification (p=0.008), clinical stage (p=0.011), and node metastasis (p=0.005) in TSCC patients. Upregulation of IGHG1 with lentivirus infection significantly increased Janus kinase 1 (JAK1) expression and the phosphorylation level of signal transducer and activator of transcription 5 (STAT5). In addition, IGHG1 overexpression markedly enhanced cell proliferation, clone formation and tumorigenesis and inhibited cell apoptosis, whereas these effects were abolished when JAK1 was downregulated in SCC15 and SCC4 TSCC cell lines. Conclusions: Collectively, this study reveals that IGHG1 functions as an oncogene in TSCC via activating JAK1/STAT5 signaling. 

Retracted: Yes

PubPeer comments:
 Figure 1B and 1D. The authors seems to accidentally regard different tailoring as different results. ![file] , 
 #1 I am very happy to receive your letter. We will repeat this experiment in response to your questions and send you the results and the original image. , 
 Withdrawn [February 2021] .  The article u201cIGHG1 functions as an oncogene in tongue squamous cell carcinoma via JAK1 STAT5 signaling, by Y.-L. Zheng, Y.-Y. Li, J.-F. Xie, H.-Q. Ma, published in Eur Rev Med Pharmacol Sci 2020; 24 (12): 6716-6725u2013DOI: 10.26355 eurrev_202006_21659u2013PMID: 32633362u201d has been withdrawn from the authors stating that u201cthe experimental data in the article are wrongu201d. The Publisher apologizes for any inconvenience this may cause. ,