PReD-Bench/PRed-Bench huggingface dataset:
Long Noncoding RNA CAT104 Promotes Cell Viability, Migration, and Invasion in Gastric Carcinoma Cells Through Activation of MicroRNA-381-Inhibiting Zinc Finger E-box-Binding Homeobox 1 (ZEB1) Expression
Authors: Gang Yuan
Qunying Wang
Dongfang Dong
Jingzi Quan
Journal: Oncology research (2018)
Discipline: CLINICAL MEDICINE
Keywords: Gastric carcinoma; biomarkers; long noncoding RNA; CAT104; miR-381
Affiliations: Department of Gastroenterology, 401 Hospital of People’s Liberation Army, Qingdao, P.R. China

Abstract:  Gastric carcinoma (GC) remains the second leading cause of cancer-related deaths worldwide. Good biomarkers are of paramount importance for GC therapy. This study aimed to assess the role of long noncoding RNA (lncRNA) CAT104 in GC. We found that CAT104 was highly expressed in human GC NCI-N87, SGC7901, BGC823, BGC803, and AGS cells. Suppression of CAT104 decreased NCI-N87 cell viability, migration, and invasion, but promoted apoptosis. CAT104 knockdown enhanced the expression of microRNA-381 (miR-381) expression in NCI-N87 cells. miR-381 participated in the regulatory effects of CAT104 on NCI-N87 cell viability, migration, invasion, and apoptosis. Zinc finger E-box-binding homeobox 1 (ZEB1) was identified as a direct target of miR-381. Overexpression of ZEB1 reversed the miR-381 mimic-induced cell viability, migration, and invasion inhibition. Suppression of ZEB1 reversed the miR-381 inhibitor-induced activation of the c-Jun N-terminal kinase (JNK) pathway and Wnt/β-catenin signaling pathways in NCI-N87 cells. In conclusion, CAT104 might function as an oncogenic factor in GC cells via regulating the expression of miR-381 and ZEB1. 

Retracted: No

PubPeer comments:
 This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: * https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) * https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: * Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 * Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 ,
The N-terminal coiled-coil domain of the cytohesin/ARNO family of guanine nucleotide exchange factors interacts with Galphaq
Authors: Emilie Dupré
Patrick M Giguère
Jean-Luc Parent
Gilles Dupuis
Geneviève Laroche
Journal: Molecular and Cellular Biochemistry (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cytohesins; G protein-coupled receptors; Galphaq; ARF6; Arf-GEF
Affiliations: Division of Rheumatology, Department of Medicine, Faculty of Medicine, Centre de Recherche Clinique Etienne-Lebel, University of Sherbrooke, 3001, 12th Avenue North, J1H 5N4 Fleurimont, Sherbrooke, QC, Canada.

Abstract:  Cytohesins are guanine-nucleotide exchange factors (GEF) for the Arf family of GTPases. One member of the Arf family, ARF6, plays an active role in the intracellular trafficking of G protein-coupled receptors. We have previously reported that Galphaq signaling leads to the activation of ARF6, possibly through a direct interaction with cytohesin-2/ARNO. Here, we report that Galphaq can directly interact with cytohesin-1, another Arf-GEF of the ARNO/cytohesin family. Cytohesin-1 preferentially associated with a constitutively active mutant of Galphaq (Galphaq-Q209L) compared to wild-type Galphaq in HEK293 cells. Stimulation of TPbeta, a Galphaq-coupled receptor, to activate Galphaq resulted in the promotion of a protein complex between Galphaq and cytohesin-1. Confocal immunofluorescence microscopy revealed that wild-type Galphaq and cytohesin-1 co-localized in intracellular compartments and at or near the plasma membrane. In contrast, expression of Galphaq-Q209L induced a drastic increase in the localization of cytohesin-1 at the plasma membrane. Expression of a dominant-negative mutant of cytohesin-1 reduced by 40% the agonist-induced internalization of TPbeta, a process that we previously demonstrated to be dependent on Galphaq-mediated signaling and Arf6 activation. Using deletion mutants, we show that cytohesin-1 interacts with Galphaq through its N-terminal coiled-coil domain. Cytohesin-1 and cytohesin-2/ARNO mutants lacking the coiled-coil domain were unable to relay Galphaq-mediated activation of Arf6. This is the first report of an interaction between the coiled-coil domain of the cytohesin/ARNO family of Arf-GEFs and a member of the heterotrimeric G proteins. 

Retracted: No

PubPeer comments:
 * Red boxes: Four lanes in the bottom panel of Figure 1A look similar to four lanes in the bottom panel of Figure 1C. Reported to the journal in October 2015, but no response as of today. ![file] ,
Asparagus Polysaccharide inhibits the Hypoxia-induced migration, invasion and angiogenesis of Hepatocellular Carcinoma Cells partly through regulating HIF1α/VEGF expression via MAPK and PI3K signaling pathway
Authors: Dongwei Xing
Lingling Weng
Wei Cheng
Ziwei Cheng
Minguang Zhang
Journal: Journal of Cancer (2021)
Discipline: CLINICAL MEDICINE
Keywords: HIF-1α; VEGF; asparagus polysaccharide; hepatocellular carcinoma.
Affiliations: Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, China., Nanjing Hospital of Chinese Medicine affiliated to Nanjing University of Chinese Medicine, Nanjing 210001, China.

Abstract:  Aim: Although there are so many treatment strategies used for hepatocellular carcinoma (HCC), the overall survival (OS) of HCC patients still remains very low. In our previous studies, asparagus polysaccharide (ASP) has been demonstrated to suppress proliferation, migration, invasion and angiogenesis of HCC cells under normoxic conditions in vitro. However, the inhibitory effects of ASP on the hypoxia-induced migration, invasion and angiogenesis of HCC cells still remain largely unexplored. Materials and methods: Cell Counting Kit-8 (CCK-8) assay, transwell assay, and tube formation assay were used to determine the effects of ASP on hypoxia-induced proliferation, migration, invasion and angiogenesis of HCC cells. ELISA, Western blotting analysis and immunofluorescence assay were used to confirm the effects of ASP on the expressions of HIF-1α and VEGF at the protein level. Moreover, effects of ASP on signaling pathway-related proteins were investigated by Western blotting analysis. Immunohistochemistry (IHC) assay was applied to test the effects of ASP on angiogenesis-associated proteins of tumor cells. Results: We showed that ASP effectively suppressed hypoxia-induced proliferation, migration, invasion and angiogenesis of SK-Hep1 and Hep-3B cells in a dose-dependent manner. In addition, the inhibitory effect of ASP might be partly attributed to down-regulation of HIF1α and VEGF proteins in SK-Hep1 and Hep-3B cells under hypoxic conditions. Moreover, signaling pathway study indicated that ASP significantly down-regulated the hypoxia-induced expressions of p-AKT, p-mTOR and p-ERK, while it had little effects on AKT, mTOR and ERK. Besides, SK-Hep1 xenograft tumor models in nude mice further confirmed that the inhibitory effect of ASP on xenograft tumors might be exerted partly via down-regulation of HIF1α and VEGF through blocking MAPK and PI3K signaling pathways. Conclusions: Our findings suggested that ASP suppressed the hypoxia-induced migration, invasion and angiogenesis of HCC cells partly through regulating HIF-1α/VEGF expression via MAPK and PI3K signaling pathways. 

Retracted: No

PubPeer comments:
 Two images in Figure 1C appear to overlap, although the brightness appears different. *** ![file] ,
LncRNA AB073614 regulates proliferation and metastasis of colorectal cancer cells via the PI3K/AKT signaling pathway
Authors: Jinfang Xue
Fang Yin
Haoyu Kuang
Yanan Wang
Liya Liao
Xiaojun Zhou
Journal: Biomedicine & Pharmacotherapy (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Colorectal cancer; LncRNA AB073614; Metastasis; PI3K/AKT signaling pathway; Proliferation.
Affiliations: Department of Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University, No.52 Mei Hua East Road, Zhuhai 519000, Guangdong, PR China., Department of General Surgery, The Fifth Affiliated Hospital, Sun Yat-sen University, No.52 Mei Hua East Road, Zhuhai 519000, Guangdong, PR China., Department of Gastroenterology, The Fifth Affiliated Hospital, Sun Yat-sen University, No.52 Mei Hua East Road, Zhuhai 519000, Guangdong, PR China. Electronic address: .

Abstract:  The expression profiles of long noncoding RNAs (lncRNAs) in colorectal cancer (CRC) have remained unclear. LncRNA AB073614 is known to be upregulated in ovarian cancer and glioma tissues, and is associated with the occurrence and progression of those cancers. In the present study, we investigated the lncRNA AB073614 gene expression patterns in CRC cell lines and tissue samples from CRC patients, and then analyzed them for possible associations with various clinicopathological characteristics. Furthermore, the roles played by lncRNA AB073614 in CRC cell proliferation, apoptosis, cell cycle progression, migration, and invasion were examined in vitro by using gene knockdown and overexpression techniques. We detected the levels of lncRNA AB073614 in 28 paired CRC tissues and adjacent normal tissues by qRT-PCR, and our results revealed that AB073614 expression in 85.7% (24/28) of the CRC tissues was significantly higher than those in the paired normal tissues. Furthermore, the levels of AB073614 were closely related to tumor grade, size, cell differentiation status, and the presence of distant metastases. Knockdown of AB073614 expression significantly inhibited the proliferation, migration, and invasion of SW480 cells, and resulted in their increased rates of apoptosis and G1 phase cell cycle arrest, whereas overexpression of AB073614 produced the opposite effects. Finally, results of studies which used an agonist (740Y-P) and an inhibitor (LY294002) of the PI3K/AKT signaling pathway, as well as the results of western blot assays, indicated that lncRNA AB073614 exerts its effects by targeting the PI3K/AKT-mediated signaling pathway. Taken together, our data indicate that lncRNA AB073614 acts to prevent CRC progression by affecting the PI3K/AKT signaling pathway, and may be useful as a novel prognostic or treatment agent for CRC. 

Retracted: No

PubPeer comments:
 Figure 3 and Figure 6 appear to have some images which overlap, in after flipping, and also resizing in some cases. Difficult to see how these apparent errors could occur solely because of confusion during figure assembly. *** ![file] ,
SREBP1 promotes the invasion of colorectal cancer accompanied upregulation of MMP7 expression and NF-κB pathway activation
Authors: Xinyi Liu
Xiaoqin Mu
Huifen Zhu
Tianyue Yang
Yuyan Gao
Binbin Liu
Xinjue Shi
Bingqing Yao
Xianxiu Nan
Shulin Liu
Yiting Hu
Journal: BMC Cancer (2019)
Discipline: CLINICAL MEDICINE
Keywords: CRC; Invasion; MMP7; NF-κB; SREBP1.

Abstract:  Background: Sterol-regulatory element binding protein 1 (SREBP1), an intracellular cholesterol sensor located in the endoplasmic reticulum, regulates the intracellular cholesterol by the Insig-Srebp-Scap pathway. Over-expression of SREBP1 can cause dyslipidemia. SREBP1 can regulate the metabolic pathway, and then promote the proliferation of tumor cells. However, there is no relevant research of metastasis and invasion in the field of colorectal cancer (CRC). Methods: Expression of SREBP1 was manipulated in CRC cell lines with low and high level SREBP1 expression by transfectiong with plasmids containing the SREBP1 gene, or by shRNA. The effect of SREBP1 on cell migration was assayed. The expression of SREBP1, p65 and MMP7 were detected by western blot. Human umbilical vein endothelial cell was used for detection of angiogenesis by adding the culture supernatant from HT29 and SW620. The level of reactive oxygen species (ROS) was detected by Dihydroethidium (DHE) staining. NF-κB inhibitor SN50 was used to test the relationship of SREBP1, NF-κB pathway and MMP7. Results: We found that the expression of SREBP1 in colon adenocarcinoma was significantly higher than that in noncancerous tissues, especially in the invasive tumor front including tumor budding. In vitro, SREBP1 over-expressed in colon cancer cell lines HT29 promoted angiogenesis in endothelial cells, increased ROS levels, phosphorylation of NF-κB-p65 and increases MMP7 expression. The effect of SREBP1 on expression of MMP7 was lost following treatment with the NF-κB inhibitor SN50. Conclusion: Our results suggest that SREBP1 can promote the invasion and metastasis of CRC cells by means of promoting the expression of MMP7 related to phosphorylation of p65. 

Retracted: No

PubPeer comments:
 In Figure 4A and E, part of a Western blot has been shared (MMP7 vs B-ACTIN). ![file] ,
ADAMTS8 Inhibits Cell Proliferation and Invasion, and Induces Apoptosis in Breast Cancer
Authors: Jianfeng Zhang
Guanglin Wang
Guiying Wang
Kun Zhang
Hongqin Ma
Jinchuan Xi
Ruoxi Tian
Xuhua Hu
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: ADAMTS8; BC; apoptosis; breast cancer; invasion
Affiliations: General Surgical Department, The Third Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China., Basic Medical College, Tianjin Medical University, Tianjin, People's Republic of China., General Surgical Department, The Fourth Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.

Abstract:  Introduction: A disintegrin and metallopeptidase with thrombospondin motifs (ADAMTSs), whose expression is dysregulated in various cancers, is implicated in cancer development. Herein, we aimed to investigate the functional role of ADAMTS8 in breast cancer (BC) and explore the underlying mechanisms. Methods: The protein expression of ADAMTS8 in BC cell lines and tumor tissues from BC patients was quantified by Western blot. ADAMTS8 overexpression was induced by transfection with pEZ-M90-ADAMTS8 plasmid using lipofectamine 2000. To generate ADAMTS8 stable knockdown cells, MDA-MB-231 cells were transfected with psi-H1-ADAMTS8siRNA plasmids. Cell counting kit-8 (CCK-8) assay, wound-healing assay, transwell assay and flow cytometry assay were employed to analyze the effects of ADAMTS8 on the proliferation, migration, invasion and apoptosis of BC cells. Chemosensitivity also was assessed using CCK-8 assay. The expressions of β-catenin, MMP-7 and c-Myc were measured by Western blot. Results: Our results showed that ADAMTS8 expression was significantly lower in BC tissues than that in adjacent non-tumor tissues. Overexpression of ADAMTS8 in MDA-MB-453 cells could inhibit the cell proliferation, migration and invasion and promote apoptosis. ADAMTS8 knockdown displayed the reverse effect in MDA-MB-231 cells. Consistently, in vivo data showed that ADAMTS8 overexpression led to a reduction in tumor growth. In addition, chemosensitivity testing in MDA-MB-453 cells transfected with pEZ-M90-ADAMTS8 plasmid indicated that cisplatin inhibited cell growth dramatically. Furthermore, attenuated β-catenin, MMP-7 and c-Myc level was detected after ADAMTS8 overexpression. Conclusion: These results indicate that increased ADAMTS8 expression could modify the progression of BC by inhibiting cell proliferation and invasion while promoting the apoptosis of BC cells. Thus, ADAMTS8 represents a potential therapeutic target for BC therapy. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have an image duplication ![file] ,
Zebrafish Noxa promotes mitosis in early embryonic development and regulates apoptosis in subsequent embryogenesis
Authors: L Zhou
Y Wang
J-X Zhong
Z Li
J-F Gui
Journal: Cell Death and Differentiation (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Noxa; apoptosis; immune system; embryo development; zebrafish
Affiliations: State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Graduate University of the Chinese Academy of Sciences, Wuhan, China.

Abstract:  Noxa functions in apoptosis and immune system of vertebrates, but its activities in embryo development remain unclear. In this study, we have studied the role of zebrafish Noxa (zNoxa) by using zNoxa-specifc morpholino knockdown and overexpression approaches in developing zebrafish embryos. Expression pattern analysis indicates that zNoxa transcript is of maternal origin, which displays a uniform distribution in early embryonic development until shield stage, and the zygote zNoxa transcription is initiated from this stage and mainly localized in YSL of the embryos. The zNoxa expression alterations result in strong embryonic development defects, demonstrating that zNoxa regulates apoptosis from 75% epiboly stage of development onward, in which zNoxa firstly induces the expression of zBik, and then cooperates with zBik to regulate apoptosis. Moreover, zNoxa knockdown also causes a reduction in number of mitotic cells before 8 h.p.f., suggesting that zNoxa also promotes mitosis before 75% epiboly stage. The effect of zNoxa on mitosis is mediated by zWnt4b in early embryos, whereas zMcl1a and zMcl1b suppress the ability of zNoxa to regulate mitosis and apoptosis at different developmental stages. In addition, mammalian mouse Noxa (mNoxa) mRNA was demonstrated to rescue the arrest of mitosis when zNoxa was knocked down, suggesting that mouse and zebrafish Noxa might have similar dual functions. Therefore, the current findings indicate that Noxa is a novel regulator of early mitosis before 75% epiboly stage when it translates into a key mediator of apoptosis in subsequent embryogenesis. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Myocardial infarction associated transcript (MIAT) promotes papillary thyroid cancer progression via sponging miR-212
Authors: Linlin Ji
Lin Bai
Qiang Wen
Lina Zhao
Renjie Wang
Journal: Biomedicine & Pharmacotherapy (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Long non-coding RNA; MIAT; Papillary thyroid cancer; ceRNA; miR-212.
Affiliations: Department of Nuclear Medicine, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China., Department of Thyroid Surgery, China-Japan Union Hospital of Jilin University, 126 XiantaiStreet, ErDao District, Changchun 13033, China., Department of Nuclear Medicine, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, ErDao District, Changchun 13033, China. Electronic address: .

Abstract:  The long noncoding RNA myocardial infarction associated transcript (MIAT) was reported to be involved in the progression of multiple cancers. However, the exact roles and molecular mechanisms of MIAT in papillary thyroid cancer (PTC) progression are still unknown. We examined the expression levels of lncRNA MIAT in 50 paired PTC tissue specimens and four PTC cell lines by real time quantitative PCR (qRT-PCR). Cell counting kit 8, colony formation, wound healing and transwell assays were performed to examine the effect of MIAT on proliferation, colony formation, migration and invasion. Tumor xenograft models were created to detect the role of MIAT in vivo tumorigenesis. The target relationships were predicted by miRcode algorithm, and confirmed by dual luciferase reporter gene assay and qRT-PCR. We found that MIAT was up-regulated in PTC tissues and cell lines. High MIAT expression was positively associated with advanced tumor-node-metastasis (TNM) stage and lymph node metastasis. Functional assays showed that knockdown of MIAT in PTC cells significantly inhibited cell proliferation, colony formation, migration and invasion in vitro, as well as impaired tumor growth in vivo. Luciferase assays further confirmed that miR-212 interacts with MIAT. Additionally, the negatively correlation of miR-212 with MIAT was verified in patients' samples. Repression of miR-212 partly abrogated the inhibitory effects of MIAT knockdown on PTC cells. Taken together, these results indicated that MIAT might be an oncogenic lncRNA that promoted PTC progression, and might be a potential therapeutic target for PTC. 

Retracted: No

PubPeer comments:
 Fig 2C.  The relative expression of MIAT in TPC-1 cells transfected with sh-MIAT or sh-NC plasmid. ... colony formation ... detected in TPC-1 cells transfected with sh-MIAT or sh-NC . ![file] Coloured boxes added. ,
LncRNA XIST inhibits hypoxia-induced cardiomyocyte apoptosis via mediating miR-150-5p/Bax in acute myocardial infarction
Authors: W-J Cui
B-P Yang
J Zhou
D Li
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Acute myocardial infarction; Long non-coding RNAs; lncRNA X inactive specific transcript (XIST); H9c2 cells; Hypoxia-induced injury
Affiliations: Department of Cardiovascular, Gansu Provincial Hospital of TCM, Lanzhou, P.R. China. .

Abstract:  Objective: Acute myocardial infarction (AMI) contributes to long-term cardiac ischemia induced by hypoxia. Long non-coding RNAs (lncRNAs) affect the development and progression of heart diseases. This study explored the role and mechanism of lncRNA X inactive specific transcript (XIST) in H9c2 cells with hypoxia-induced injury. Materials and methods: Methyl-thiazolyl-tetrazolium (MTT), transwell, and flow cytometry assays were employed to analyze the survival, invasion, migration, and apoptosis of H9c2 cells under different conditions, respectively. Expression of related genes was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) or Western blot. Results: XIST was over-expressed in H9c2 cells with hypoxia-induced injury, and the silence of XIST alleviated cell injury. Up-regulation of XIST promoted the expression of B-cell lymphoma 2-Associated X (Bax) through competitive binding to miR-150-5p. Conclusions: XIST protects cardiomyocytes from hypoxia-induced injury by mediating miR-150-5p/Bax axis, suggesting that XIST is an important target for AMI treatment. 

Retracted: No

PubPeer comments:
 ![file] Fig3E, lots of repetitive features in the background. Could the corresponding author elaborate on how these repetitive features are present in different protein detections? , 
 ![file] , 
 I agree with both comments, but comment #1 refers to Figure 2D and comment #2 to Figure 3E, at least in the PDF copy that I downloaded. Figure 5H and 6D show the same  stamping of several patterns. I have highlighted the Two Jumping Dolphins with orange ellipses and the Eiffeltower with dark orange squares. I will leave the rest for others. ![file] The flow cytometry panels all look very similar as well, and have an unexpected granular pattern. ![file] The repeating background patterns and strangely curved Western blots bands, in conjunction with the specific title structure, anonymous email address, topic of study (LncRNA) and artificial looking flow cytometry plots all point towards a Paper Mill Production. Of course the authors could prove me wrong by showing uncropped Western blots or other raw data. , 
 #3 ![] The same periodic background mottled pattern has affected the WB slices in [Li et al (2020)] - different authors working at a different institution. ![] Li et al also present flow-cytometry plots of similar appearance to the current examples, with the same peculiar half-tone texture, as if seen through the texture of fabric. ![] ,
Enrichment and characterization of cancer stem-like cells in ultra-low concentration of serum and non-adhesive culture system
Authors: Chuanping Si
Junfeng Zhang
Lei Dai
Zhaochen Ning
Hui Zhang
Huabao Xiong
Chunlei Li
Lin Cheng
Wei Xu
Yunsheng Zhang
Guanjun Dong
Fenglian Yan
Hui Shi
Hongxin Deng
Journal: American journal of translational research (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cancer stem cells; cancer; characterization; marker.
Affiliations: Institute of Immunology and Molecular Medicine, Jining Medical University Jining 272067, Shandong, China., State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University Chengdu, Sichuan, China., School of Pharmacy, Linyi University Linyi 276000, Shandong, China., Shenzhen SiBiono GeneTech Co. Ltd. Shenzhen, China., Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai New York, NY 10029, USA.

Abstract:  Cancer stem cells (CSCs) play important roles in tumor initiation, metastasis, and progression. They are also mainly responsible for high treatment failure rates. Identification and characterization of CSCs are crucial for facilitating the detection, prevention, or therapy of cancer. Great efforts have been paid to develop an effective method and the ideal method for CSCs research is still in the going. In our study, we created an ultra-low concentration of serum and non-adhesive (ULCSN) culture system to enrich CSCs from murine lewis lung cancer cell line LL/2 with cell spheres structure and characterize the LL/2 CSCs properties. Their characteristics were investigated through colony formation, spheres formation, chemoresistance, flow cytometry for putative stem cell markers, such as CD133, CD34 and CD45, immunofluorescence staining and tumor initiation capacity in vivo. Tumor spheres were formed within 7-10 days under the condition of ULCSN culture system. Compared with adherent parental LL/2 cells, the colony capacity, chemo-resistance, and expression of stem cell markers increased significantly in addition to tumor-initiating capability in the tumor sphere cells. Using the ULCSN culture system, an available isolation method of lewis lung CSCs was established, which is simple, effective, and inexpensive compared with the cytokines attachment serum free culture method. The stem cell properties of the tumor sphere LL/2 cells reflected the CSCs phenotypes. We developed a useful CSCs model for basic and pre-clinical studies for lung cancer and other types of cancer. 

Retracted: No

PubPeer comments:
 Fig 5 has several unexpected duplicates. Please make comments. Thanks!![file] , 
 Dear Dr. Lycoperdon Lividum, Thank you very much for pointing out the mistakes of Figure 5 in our published work. We have carefully investigated our raw data and found that these errors were inadvertently made during the preparation of the manuscript. We will contact the journal editorial office as soon as possible to correct the errors. Thank you again for helping us find and correct the mistakes. Sincerely yours Zhang Junfeng ,
MicroRNA-139-5p Suppresses 3T3-L1 Preadipocyte Differentiation Through Notch and IRS1/PI3K/Akt Insulin Signaling Pathways
Authors: Lin Mi
Qiangling Zhang
Xueli Zheng
Delin Mo
Yaosheng Chen
Gongshe Yang
Youlei Li
Journal: Journal of cellular biochemistry (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 3T3-L1; ADIPOCYTE DIFFERENTIATION; IRS1/PI3K/Akt INSULIN SIGNALING; NOTCH SIGNALING; miR-139-5p.
Affiliations: Laboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, Yangling, China., College of Life Science, Sun Yat-Sen University, Guangzhou, China., College of forestry, Northwest A&F University, Yangling, China.

Abstract:  MicroRNAs (miRNAs) participate in the regulation of adipogenesis. Identification of the full repertoire of miRNAs expressed in adipose tissue is likely to significantly improve our understanding of adipose tissue growth and development. Here, miR-139-5p was identified as an inhibitor of 3T3-L1 adipocyte differentiation with significantly down-regulating the expression levels of adipogenic marker genes PPAR γ (P &lt; 0.01), aP2 (P &lt; 0.01) and FAS (P &lt; 0.01). Importantly, flow cytometry and EdU incorporation assay indicated that this inhibition was partly due to the dysfunction of clonal expansion. Furthermore, we firstly demonstrated that miR-139-5p blocked adipogenesis via directly targeted the 3' untranslated regions (UTRs) of Notch1 and IRS1 mRNAs, a key member of Notch signaling and IRS1/PI3K/Akt insulin signaling, respectively. In addition, the overexpression of Notch1 or IRS1 partially restored the suppressive effects miR-139-5p on differentiation of 3T3-L1 cells. To our knowledge, this was the first report that miR-139-5p functioned negatively by targeting Notch1 and IRS1 during 3T3-L1 adipogenesis, regulating the transition from clonal expansion to terminal differentiation. 

Retracted: No

PubPeer comments:
 Figure 1C. IkappaBalpha panel. Light streaks between bands. ERK 1 2 Thr202?Tyr204 and ERK 1 2 panels do not look like they come from the same blot. ![file] ,
Mouse model of ocular hypertension with retinal ganglion cell degeneration
Authors: Kip M Connor
Meredith Gregory-Ksander
Joan W Miller
Ryo Mukai
Yoko Okunuki
Anitha Krishnan
Deeba Husain
Garrett Klokman
Dong Ho Park
Clifford B Kim
Eiichi Hasegawa
Journal: PLoS ONE (2019)
Discipline: Multidisciplinary
Keywords: Ocular hypertension; Glaucoma; Retinal ganglion cell degeneration; Mouse model; Intraocular pressure
Affiliations: Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye & Ear Infirmary, Harvard Medical School, Boston, Massachusetts, United States of America., Department of Ophthalmology, Graduate School of Medical Sciences, Gunma University, Maebashi, Gunma, Japan., Department of Ophthalmology, School of Medicine, Kyungpook National University, Kyungpook National University Hospital, Jung-gu, Daegu, South Korea., Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka-city, Fukuoka, Japan., Schepens Eye Research Institute of Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States of America.

Abstract:  Objectives: Ocular hypertension is a primary risk factor for glaucoma and results in retinal ganglion cell (RGC) degeneration. Current animal models of glaucoma lack severe RGC cell death as seen in glaucoma, making assessment of physiological mediators of cell death difficult. We developed a modified mouse model of ocular hypertension whereby long-lasting elevation of intraocular pressure (IOP) is achieved, resulting in significant reproducible damage to RGCs. Results: In this model, microbeads are mixed with hyaluronic acid and injected into the anterior chamber of C57BL/6J mice. The hyaluronic acid allows for a gradual release of microbeads, resulting in sustained blockage of Schlemm's canal. IOP elevation was bimodal during the course of the model's progression. The first peak occurred 1 hours after beads injection, with an IOP value of 44.69 ± 6.00 mmHg, and the second peak occurred 6-12 days post-induction, with an IOP value of 34.91 ± 5.21 mmHg. RGC damage was most severe in the peripheral retina, with a loss of 64.1% compared to that of untreated eyes, while the midperiphery exhibited a 32.4% loss, 4 weeks following disease induction. Conclusions: These results suggest that sustained IOP elevation causes more RGC damage in the periphery than in the midperiphery of the retina. This model yields significant and reproducible RGC degeneration. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have two sets of images which overlap. If I am understanding the diagram in 3A, the overlap is not intentional. *** ![file] ![file] , 
 Also, it is considered that yellow boxes in Fig.6 are similar. ![file] ,
A partially folded structure of amyloid-beta(1–40) in an aqueous environment
Authors: Jeffrey R Brender
Shirley Y Lee
Subramanian Vivekanandan
Ayyalusamy Ramamoorthy
Journal: Biochemical and Biophysical Research Communications (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Aβ(1-40); aggregation; extracellular plaques; Alzheimer's disease; structure
Affiliations: Department of Biophysics, University of Michigan, Ann Arbor, MI 48109-1055, USA.

Abstract:  Aggregation of the Aβ(1-40) peptide is linked to the development of extracellular plaques characteristic of Alzheimer's disease. While previous studies commonly show the Aβ(1-40) is largely unstructured in solution, we show that Aβ(1-40) can adopt a compact, partially folded structure. In this structure (PDB ID: 2LFM), the central hydrophobic region of the peptide forms a 3(10) helix from H13 to D23 and the N- and C-termini collapse against the helix due to the clustering of hydrophobic residues. Helical intermediates have been predicted to be crucial on-pathway intermediates in amyloid fibrillogenesis, and the structure presented here presents a new target for investigation of early events in Aβ(1-40) fibrillogenesis. 

Retracted: No

PubPeer comments:
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 I can see this is an old thread. Without going into the details of the other papers, I might point to some work we did with the lab of Dominic Walsh and published in 2014: https: pubmed.ncbi.nlm.nih.gov 24785004 Dominic was very mindful of sample conditions and made us record NMR spectra ONLY on samples that got straight off a SEC column and only for limited time - all in order to minimize contributions from dimers or higher order assemblies. In addition we were constrained to work at high pH (pH 8.0) and low temperature (278 K) to further avoid self-association. This made the NMR more challenging to do, but likely was important in the analysis and for the conclusions. Then, when it comes to the structural preferences, it is customary to report SSP (secondary structure propensities) by comparison to random coil chemical shifts . These are EXTREMELY sensitive to the reference set used. You can consult some reviews or papers about this. I will point out a recent paper from my own group here: https: pubmed.ncbi.nlm.nih.gov 34146207 and a more general review on the topic: https: pubmed.ncbi.nlm.nih.gov 32696364 . Keep in mind here that these are DEVIATIONS from the INTRINSIC distribution of Ramachandran space. Absolute measures of structure should be derived from J-couplings, RDCs and other data. Also, remain aware of the 1 r^6 nature of the NOE versus the linear averages obtained by other methods. You are welcome to consult the publications for further detail. Frans Mulder ,
Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis
Authors: Yannan Xi
Florian Wiede
Juan Sastre
Ahmed Bettaieb
Tony Tiganis
Santana Bachaalany
Ellen Hosein
Stephen M Griffey
Fawaz G Haj
Nicole Coggins
Salvador Perez
Journal: Cell Communication and Signaling (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Acute pancreatitis; T-cell protein tyrosine phosphatase; cerulein-induced; inflammatory signaling; pancreatic TCPTP
Affiliations: Department of Nutrition, University of California Davis, One Shields Ave, 3135 Meyer Hall, Davis, CA 95616, USA. .

Abstract:  Background: Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results: In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal role in AP we generated mice with pancreatic TCPTP deletion (panc-TCPTP KO) by crossing TCPTP floxed mice with Pdx1-Cre transgenic mice. Amylase and lipase levels were lower in cerulein-treated panc-TCPTP KO mice compared with controls. In addition, pancreatic mRNA and serum concentrations of the inflammatory cytokines TNFα and IL-6 were lower in panc-TCPTP KO mice. At the molecular level, panc-TCPTP KO mice exhibited enhanced cerulein-induced STAT3 Tyr705 phosphorylation accompanied by a decreased cerulein-induced NF-κB inflammatory response, and decreased ER stress and cell death. Conclusion: These findings revealed a novel role for pancreatic TCPTP in the progression of cerulein-induced AP. 

Retracted: No

PubPeer comments:
 Concern about Figure 1A and 1C: * The Tubulin panel in Figure 1A only has six lanes instead of the expected seven lanes * Red boxes: The Tubulin panel in Figure 1A appears similar to six lanes in the Tubulin panel in Figure 1C. ![file] ,
Multi-omics approach to COVID-19: a domain-based literature review
Authors: Martina Rueca
Chiara Farroni
Giulia Matusali
Alessandra Aiello
Francesca Colavita
Francesco Messina
Manuela Antonioli
Francesco Nicola Lauria
Gabriella Rozera
Giuseppe Ippolito
Alessandra Sacchi
Chiara Montaldo
Mauro Piacentini
Maria Rosaria Capobianchi
Gian Maria Fimia
Emanuela Giombini
Chiara Agrati
Delia Goletti
Fabiola Ciccosanti
Veronica Bordoni
Isabella Abbate
Saeid Najafi Fard
Journal: Journal of Translational Medicine (2021)
Discipline: CLINICAL MEDICINE
Keywords: COVID-19; Conceptual domain; Host signatures; Omics; Pathways
Affiliations: National Institute for Infectious Diseases, "Lazzaro Spallanzani" - IRCCS, Via Portuense, 292, 00149, Rome, Italy., National Institute for Infectious Diseases, "Lazzaro Spallanzani" - IRCCS, Via Portuense, 292, 00149, Rome, Italy. .

Abstract:  Background: Omics data, driven by rapid advances in laboratory techniques, have been generated very quickly during the COVID-19 pandemic. Our aim is to use omics data to highlight the involvement of specific pathways, as well as that of cell types and organs, in the pathophysiology of COVID-19, and to highlight their links with clinical phenotypes of SARS-CoV-2 infection. Methods: The analysis was based on the domain model, where for domain it is intended a conceptual repository, useful to summarize multiple biological pathways involved at different levels. The relevant domains considered in the analysis were: virus, pathways and phenotypes. An interdisciplinary expert working group was defined for each domain, to carry out an independent literature scoping review. Results: The analysis revealed that dysregulated pathways of innate immune responses, (i.e., complement activation, inflammatory responses, neutrophil activation and degranulation, platelet degranulation) can affect COVID-19 progression and outcomes. These results are consistent with several clinical studies. Conclusions: Multi-omics approach may help to further investigate unknown aspects of the disease. However, the disease mechanisms are too complex to be explained by a single molecular signature and it is necessary to consider an integrated approach to identify hallmarks of severity. 

Retracted: No

PubPeer comments:
 I saw this title and was excited to read a summary of multi-omics work related to COVID-19. After skimming the paper and the citations it quickly became clear that the article does not cite a single paper that did multi-omic analysis? In their own words from the methods, the paper is instead about:  (1) networks of virusu2013human PPIs; (2) interaction clusters of pathways, involving dynamic processes at different times, not represented in a static view. ,
Phenylephrine induces activation of CREB in adult rat cardiac myocytes through MSK1 and PKA signaling pathways
Authors: Antigone Lazou
Margarita Hadzopoulou-Cladaras
Thomais Markou
Journal: Journal of Molecular and Cellular Cardiology (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CREB; phosphorylation; phenylephrine; cardiac myocytes; alpha(1)-adrenergic receptors
Affiliations: Laboratory of Animal Physiology, Department of Zoology, School of Biology, Aristotle University of Thessaloniki, Thessaloniki 54124, Greece.

Abstract:  cAMP responsive element binding protein (CREB) is a stimulus induced transcription factor with possible relevance for the pathophysiology of the heart. In the present study, we provide evidence that the hypertrophic agonist, phenylephrine (PE), promotes phosphorylation of CREB in adult rat cardiac myocytes through alpha(1)- and beta-adrenergic receptors. PE-induced phosphorylation of CREB was partially inhibited by Ro318220 and H89, which were shown to be potent inhibitors of mitogen- and stress-activated protein kinase-1 (MSK1) activation, implicating the involvement of this kinase in the response. Similar results were obtained when cardiac myocytes were treated with the inhibitors of ERK1/2 and p38 MAPK pathways. In addition, inhibition of protein kinase A by RpcAMP reduced phosphorylation of CREB, suggesting that this pathway is also involved. Furthermore, PE stimulation was accompanied by an increase in CRE-binding activity, which was reduced by drugs that prevented phosphorylation of CREB. An enhanced CBP/phospho-CREB complex formation was also observed, suggesting recruitment of CBP to phosphorylated CREB. These results suggest that PE stimulates phosphorylation and DNA binding activity of CREB in adult rat ventricular myocytes through multiple signaling pathways involving ERK1/2, p38 MAPK, MSK1 and PKA. The same pathways seem to regulate atrial natriuretic peptide (ANF) mRNA expression, a highly conserved marker gene of cardiac hypertrophy, suggesting that the PE-stimulated activation of CREB is likely to play an important role in the hypertrophic response. 

Retracted: No

PubPeer comments:
 Figure 7a and 7b: more similar than expected ![file] , 
 Thank you for bringing this to our attention. The data is more than 15 years old and we have no digital files for this project and the figures of this paper. However, we have records of the experiments performed and hard copies of the initial agarose gels that were used for the densitometry. These files support the original data and not affect any of the original conclusions. ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ,
MiR-124 reversed the doxorubicin resistance of breast cancer stem cells through STAT3/HIF-1 signaling pathways
Authors: Yimin Wang
Yingying Wang
Caixia Guo
Zhaoying Yang
Cong Liu
Hua Xing
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HIF-1 signaling pathway; Mir-124; STAT3; breast cancer stem-like cells; doxorubicin resistance.
Affiliations: Department of Breast Surgery, China-Japan Union Hospital of Jilin University , Jilin , China., Department of Nursing, China-Japan Union Hospital of Jilin University , Jilin , China., Scientific Research Center, China-Japan Union Hospital of Jilin University , Jilin , China., The forth department of neurology, China-Japan Union Hospital of Jilin University , Jilin , China.

Abstract:  Various drug treatments including doxorubicin (DOX) have been proved efficient in the suppression of breast cancer. Nonetheless, drug resistance became an obstacle in the therapeutic process. According to recent literatures, breast cancer stem cells (BCSCs) were considered contributing to drug resistance, besides, microRNAs (miRNAs) could regulate proteins associated with drug resistance in human breast cancer. To further understand the inner mechanism of drug resistance in breast cancer and look for remedy methods, we referred to bioinformatic analysis and predicted that signal transducer and activator of transcription 3 (STAT3) and miR-124 was overexpressed in MCF7-R cells (MCF7 cells resistant to DOX) compared with MCF cells. Expression levels of RNA and protein were separately determined by qRT-PCR and western blot. Dual luciferase assay was performed to verify the targeting relationship between STAT3 and miR-124. Optical density (OD) values and apoptotic rates of cells were respectively determined via MTT assays and flow cytometric analysis. Cell invasion was detected to verify drug resistance. Results of above assays indicated that STAT3 was highly expressed in MCF7-R cells than in MCF7 cell lines and affected doxorubicin resistance of BCSCs, and miR-124 reversed the doxorubicin resistance of breast cancer stem cells through targeting STAT3 to control the HIF-1 signaling pathway. To conclude, this research may be valuable for the treatment of breast cancer as the restoration of miR-124 and inhibition of STAT3 could be applied to therapeutic strategy and help overcome drug resistance. 

Retracted: No

PubPeer comments:
 Figs 3d ( The percentage of apoptotic cells was determined by flow cytometric analysis ) and 5g ( The overexpression of miR-124 group had a greater apoptotic percentage than the MCF-R group, while the co-transfection of the miR-124 mimics and STAT3 has a similar apoptotic percentage compared with the MCF7-R group ). ![file] Two panels are almost identical (red boxes), with minor differences in the lower quadrants. ,