PReD-Bench/PRed-Bench huggingface dataset:
Insulin-like growth factor-binding protein-5 induces pulmonary fibrosis and triggers mononuclear cellular infiltration
Authors: Carol A Feghali-Bostwick
Hidekata Yasuoka
Augustine M K Choi
Joseph M Pilewski
Zhihong Zhou
Tim D Oury
Journal: American Journal Of Pathology (2006)
Discipline: CLINICAL MEDICINE
Keywords: IGFBP-5; pulmonary fibrosis; extracellular matrix; fibroblast activation; myofibroblastic changes
Affiliations: Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.

Abstract:  We have recently shown that insulin-like growth factor-binding protein (IGFBP)-5 is overexpressed in idiopathic pulmonary fibrosis lung tissues and increases collagen and fibronectin deposition. Here, we further examined the effect of IGFBP-5 in vivo by intratracheal administration of replication-deficient adenovirus expressing human IGFBP-5 (Ad5), IGFBP-3 (Ad3), or no cDNA (cAd) to wild-type mice. Increased cellular infiltration and extracellular matrix deposition were observed in mice after Ad5 administration compared with Ad3 and cAd. Mononuclear cell infiltration consisted predominantly of T lymphocytes at day 8. By day 14, the number of infiltrating T cells decreased, whereas that of B cells and monocytes/macrophages increased. IGFBP-5 also induced migration of peripheral blood mononuclear cells in vitro, suggesting that in vivo mononuclear cell infiltration may be the direct result of IGFBP-5 expression. alpha-Smooth muscle actin and Mucin-1 co-localized in cells of mice treated with Ad5, suggesting that IGFBP-5 induced epithelial-mesenchymal transition. In addition, exogenous IGFBP-5 induced alpha-smooth muscle actin expression in primary fibroblasts and epithelial-mesenchymal transition of pulmonary epithelial cells in vitro. In conclusion, our results suggest that overexpression of IGFBP-5 in mouse lung results in fibroblast activation, increased extracellular matrix deposition, and myofibroblastic changes. Thus, the IGFBP-5-induced fibrotic phenotype in vivo may represent a novel model to better understand the pathogenesis of fibrosis. 

Retracted: No

PubPeer comments:
 Figure 5. Treatments seem different, yet images very similar. https: imgur.com 7idrOYI , 
 #1 Yes, clearly.  ,
Glial Cell Line-Derived Neurotrophic Factor-Transfected Placenta-Derived Versus Bone Marrow-Derived Mesenchymal Cells for Treating Spinal Cord Injury
Authors: Huilin Yang
Hui Gao
Yao Lu
Man Zhang
Bing Chen
Journal: Medical Science Monitor (2017)
Discipline: CLINICAL MEDICINE
Keywords: Placenta-derived mesenchymal stem cells; PMSCs; glial cell line-derived neurotrophic factor; GDNF; spinal cord injury
Affiliations: Department of Orthopedics, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China (mainland)., Department of Dermatology, College of Clinical of Yangzhou University, Yangzhou, Jiangsu, China (mainland)., Comparative Medicine Center, Yangzhou University, Yangzhou, Jiangsu, China (mainland).

Abstract:  BACKGROUND Placenta-derived mesenchymal stem cells (PMSCs) were isolated from placenta and had differentiation and self-renewal potential. We transfected PMSCs with glial cell line-derived neurotrophic factor (GDNF) and compared their effect for repairing spinal cord injury (SCI) with that of GDNF-transfected bone marrow-derived mesenchymal stem cell (BMSC). MATERIAL AND METHODS The PMSCs were isolated from Sprague-Dawley rat placenta; BMSCs were isolated from Sprague-Dawley rat thigh bone marrow. Primary cultured BMSCs and PMSCs were uniformly spindle-shaped. Flow cytometry indicated that both cell types were CD29- and CD90-positive and CD34- and CD45-negative, confirming that they were MSCs. The PMSCs and BMSCs were transfected with recombinant lentivirus containing the GDNF gene in vitro. PMSC and BMSC viability was increased after transfection, and GDNF expression was increased until 10 d after transfection. SCI was created in the rats (n=64) and was repaired using transfected PMSCs and BMSCs or untransfected PMSCs and BMSCs. RESULTS The transfected PMSCs and BMSCs repaired the SCI. Flow cytometry, histology, immunohistochemical, kinesiology properties, and Basso-Beattie-Bresnahan locomotion score measurements determined no significant difference between transfected PMSCs and BMSCs at 7, 14, and 21 d post-transplantation (P&gt;0.05); the injury healed better in transfected PMSCs and BMSCs than in untransfected PMSCs and BMSCs (P&lt;0.05). CONCLUSIONS MSCs have similar biology characteristics and capacity for SCI repair to BMSCs and can be used as a new resource for treating SCI. 

Retracted: No

PubPeer comments:
 There appear to be 2 image duplications in figure 7  ,
Synergistic Combination of Doxorubicin and Paclitaxel Delivered by Blood Brain Barrier and Glioma Cells Dual Targeting Liposomes for Chemotherapy of Brain Glioma
Authors: Qin He
Mingqing Yuan
Xiaoxiao Chen
Huile Gao
Yu Ting Yang
Qianyu Zhang
Journal: Current pharmaceutical biotechnology (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Brain glioma; blood brain barrier (BBB); dual-ligand delivery; transferrin; cell-penetrating peptide
Affiliations: Key Laboratory of Drug Targeting and Drug Delivery Systems, Ministry of Education; West China School of Pharmacy, Sichuan University, No. 17, Block 3, Southern Renmin Road, Chengdu, 610041, Sichuan, P. R. China. .

Abstract:  Brain glioma has become a great threat to human health in decades. To maximize the therapeutic efficacy of brain glioma as well as minimize the side effects, drugs should be penetrated through the blood brain barrier (BBB) and then targeted to the brain carcinoma cells with effective concentration. A dual-ligand delivery strategy was employed to achieve both of these goals. Herein, both specific targeting ligand transferrin and cell-penetrating peptide TAT were conjugated onto liposomes (TF/TAT-LP) to develop a brain glioma dual-ligand delivery system. Synergistic combination of doxorubicin (DOX) and paclitaxel (PTX), compared with using them separately, could more efficiently suppress tumor aggravation. In vitro studies including cellular uptake and three-dimensional (3D) tumor spheroid penetration assays proved that TF/TAT-LP could target brain endothelial and carcinoma cells with deeply penetration through the endothelial monolayers and target to the core of the tumor spheroids. In vivo imaging proved that the TF/TAT-LP possesses the highest tumor distribution, which was also confirmed by fluorescent images of the brain section. Ultimately, the DOX and PTX-loaded TF/TAT-LP (TF/TAT-PTX/DOX-LP) shows the best anti-glioma effect with improvement of glioma bearing survival time. In conclusion, synergistic combination of doxorubicin and paclitaxel delivered by the TF/TAT-LP could efficiently target to the brain glioma with satisfying treatment efficiency, which may be a promising formulation for glioma therapy. 

Retracted: No

PubPeer comments:
  Fig. (9). Micrograph of histopathology section of heart tissue (HE, u00d7 100). a=saline, b=Free DOX, c=Free PTX DOX, d=PEG-PTX DOX-LP, e=TF-PTX DOX-LP, f=TAT-PTX DOX-LP, g=TF TAT-DOX-LP, h=TF TAT-PTX DOX-LP. Arrows pointed to the damaged area. Overlap marked.  , 
  Fig. (7). The representative in vivo (A) [...] images of C6 tumor-bearing BALB C mice after injection of DIR-labeled liposomes. I urge the authors to check the mouse images.  ,
Cytochrome P450 genes are differentially expressed in female and male hepatocyte retinoid X receptor alpha-deficient mice
Authors: Tamiko Konishi
Yan Cai
Tiane Dai
Chawnshang Chang
Kuang-Hsiang Chuang
Yanhe Lue
Yu-Jui Yvonne Wan
Yan Ao
Journal: Endocrinology (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: retinoid X receptor alpha; hepatocytes; CYP450 genes; male mice; female mice
Affiliations: Departments of Pathology (Y.C., T.D., Y.A., T.K., Y.-J.Y.W.), Harbor-University of California, Los Angeles Medical Center, Torrance, California 90509, Department of Pathology (K.-H.C., C.C.), University of Rochester, Rochester, New York 14642;, Medicine (Y.L.), Harbor-University of California, Los Angeles Medical Center, Torrance, California 90509

Abstract:  To study the functional role of retinoid X receptor alpha (RXRalpha) in hepatocytes, hepatocyte RXRalpha-deficient mice have been established. Characterization has been performed on male mice. In this paper, we show that the expression of CYP450 genes is differentially expressed in male and female hepatocyte RXRalpha-deficient mice; male mice have reduced expression of cytochrome P450 (CYP) CYP4A, CYP3A, and CYP2B mRNAs, but females do not exhibit such phenotypes. To examine the hormonal effects on this sexual dimorphic phenotype, male and female mice were subjected to 17beta-estradiol and 5alpha-dihydrotestosterone (DHT) treatment, respectively, and then the expression of the CYP450 genes was studied. Estradiol had no effect on protecting the hepatocyte RXRalpha-deficient mice from reduced expression of the CYP450 genes. In contrast, DHT induced hepatocyte RXRalpha-deficient female mice, but not wild-type female mice, to have the reduced expression of CYP450 mRNAs. In addition, castration prevented the mutant male mice from exhibiting reduced expression of CYP450 mRNAs. wild-type and mutant mouse livers from both genders express androgen receptors (ARs). By transient transfection, DHT-AR could inhibit RXRalpha-mediated transcription. Furthermore, by transfection and coimmunoprecipitation, RXR can interact with AR in vivo. These data suggest that testosterone has a negative impact on retinoid signaling when the level of RXRalpha is low, which may in turn reduce the expression of the CYP450 genes. 

Retracted: No

PubPeer comments:
 Figure 3. Some panels look more similar to each other than expected. Panels that look similar are highlighted with boxes of the same color.  Here is a Fiji false color analysis which seems to support the similarities.  , 
 Figure 5. Some actin panels here also look more similar than expected, but the resolution is low. In addition, actin panels that were expected to look similar between A and B, actually look different.  ,
Circular RNA circ-SMAD7 promoted glioma cell proliferation and metastasis by upregulating PCNA
Authors: J Lu
C-Y Zuo
W Qian
C-J Huang
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: circ-SMAD7; glioma; tumor progression; cell proliferation; cell cycle
Affiliations: Department of Neurosurgery, The Ninth People's Hospital of Suzhou, Suzhou, China. .

Abstract:  Objective: Recent studies have discovered a class of circular RNAs (circRNAs), which are dysregulated in various tumors and participate in the regulation of tumor progression. In our research, we aim to research the function of circ-SMAD7 in the progression of glioma. Patients and methods: Circ-SMAD7 expression was detected by quantitative Real Time Polymerase Chain Reaction (qRT-PCR) in glioma tissue patients. Pearson's Chi-square test was used to determine the association of circ-SMAD7 expression with several clinicopathological factors. Besides, cell proliferation assay, cell cycle assay, transwell assay, and Matrigel assay were conducted to detect the function of circ-SMAD7 in glioma. In addition, the interaction between circ-SMAD7 and proliferating cell nuclear antigen (PCNA) in glioma was studied by performing qRT-PCR and Western blot assay. Results: Circ-SMAD7 expression was observed in glioma tissues when compared with adjacent samples. The expression of circ-SMAD7 was associated with patients' WHO stage and KPS score. Cell proliferation was inhibited and cell cycle was regulated after circ-SMAD7 was downregulated in glioma cells. Besides, cell migration and invasion were inhibited after circ-SMAD7 was downregulated in glioma cells. In addition, the mRNA and protein expression of PCNA was repressed after circ-SMAD7 was knocked down in glioma cells. Furthermore, PCNA expression level positively correlated to circ-SMAD7 expression level in glioma samples. Conclusions: Our study suggests that circ-SMAD7 promotes proliferation and metastasis of glioma via upregulating PCNA. Circ-SMAD7/ PCNA might be a novel therapeutic strategy in glioma. 

Retracted: Yes

PubPeer comments:
 Figure 2A appears to have two bands (one MM patient responder (R) and one non-responder (NR)) that when flipped horizontally share unexpected similarities, including surrounding background features. *** Inverted for illustration  *** Original  ,
Ursodeoxycholic acid stimulates alveolar fluid clearance in LPS‚Äêinduced pulmonary edema via ALX/cAMP/PI3K pathway
Authors: Lingling Sun
Rong Zhang
Ning Gan
Xiaotao Xu
Fangfang Niu
Aizhong Wang
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Na+/K+-ATPase; alveolar fluid clearance; epithelial sodium channel; pulmonary edema; ursodeoxycholic acid.
Affiliations: Department of AnesthesiologyShanghai Jiao Tong University Affiliated Sixth People's HospitalShanghai China

Abstract:  This study aims to examine the impact of ursodeoxycholic acid (UDCA) on pulmonary edema and explore the underlying molecular mechanisms. The effects of UDCA on pulmonary edema were assessed through hematoxylin and eosin (H&amp;E) staining, lung dry/wet (W/D) ratio, TNF-Œ±/IL-1Œ≤ levels of bronchoalveolar lavage fluid (BALF), protein expression of epithelial sodium channel (ENaC), and Na+ /K+ -ATPase. Besides, the detailed mechanisms were explored in primary rat alveolar type (AT) II epithelial cells by determining the effects of BOC-2 (ALX [lipoxin A4 receptor] inhibitor), Rp-cAMP (cAMP inhibitor), LY294002 (PI3K inhibitor), and H89 (PKA inhibitor) on the therapeutic effects of UDCA against lipopolysaccharide (LPS)-induced changes. Histological examination suggested that LPS-induced lung injury was obviously attenuated by UDCA. BALF TNF-Œ±/IL-1Œ≤ levels and lung W/D ratios were decreased by UDCA in LPS model rats. UDCA stimulated alveolar fluid clearance (AFC) though the upregulation of ENaC and Na+ /K+ -ATPase. BOC-2, Rp-cAMP, and LY294002 largely suppressed the therapeutic effects of UDCA. Significant attenuation of pulmonary edema and lung inflammation was revealed in LPS-challenged rats after the UDCA treatment. The therapeutic efficacy of UDCA against LPS was mainly achieved through the ALX/cAMP/PI3K pathway. Our results suggested that UDCA might be a potential drug for the treatment of pulmonary edema induced by LPS. 

Retracted: No

PubPeer comments:
 In Figure 2b, a micrograph has been duplicated, manipulated and presented as something else.  ,
Combining sorafenib with celecoxib synergistically inhibits tumor growth of non-small cell lung cancer cells in vitro and in vivo
Authors: Kaizhong Wang
Zhihong Li
Hong Zhang
Journal: Oncology Reports (2014)
Discipline: CLINICAL MEDICINE
Keywords: COX-2; VEGFR; sorafenib; celecoxib; NSCLC
Affiliations: Department of Thoracic Surgery, The First Hospital, Jilin University, Chaoyang, Changchun, Jilin 130021, P.R. China.

Abstract:  Although inhibition of cyclooxygenase-2 (COX-2) or the vascular endothelial growth factor receptor (VEGFR) has been shown to be a promising antitumor strategy in non-small cell lung cancer (NSCLC), the therapeutic efficacy is limited due to inherent tumor resistance. In the present study, we selected sorafenib (SOR), a VEGFR inhibitor, in combination with celecoxib (CXB), a COX-2 inhibitor, for suppressing tumor growth and simultaneously for reducing doses of both drugs for the treatment of NSCLC. The effects of SOR combined with CXB were examined in A549 cells (an NSCLC cell line). Assays of proliferation, apoptosis, cell cycle distribution and receptor signaling were performed. We found that treatment with the combination of low concentrations of SOR and CXB significantly suppressed the proliferation of A549 tumor cells in vitro and suppressed tumor growth in vivo when compared to the actions of either agent alone. The results also showed that the combination of SOR and CXB significantly increased the induction of apoptosis and decreased the expression of inhibitor of apoptosis genes, survivin and Bcl-2 (p&lt;0.01). Furthermore, the combination treatment significantly suppressed constitutive phosphorylation of MEK and ERK, which may contribute to the inhibition of tumor growth. Taken together, our findings revealed that this additive combination of SOR and CXB is a potential drug candidate for the treatment of NSCLC. 

Retracted: No

PubPeer comments:
 *[left]* Fig 4.  Combination of sorafenib and celecoxib inhibits RAF MEK ERK signaling in A549 cells. Cells were treated with sorafenib and celecoxib or both for 2 h. Western blot analysis was performed using specific antibodies against the indicated proteins. Blots were reprobed for u03b2-actin to normalize each lane for protein content . *[right]* Fig 3C from [Qian et al (2014)] .  MMP-2 and MMP-9 expression was determined 72 h after treatment with CET and CXB alone or the combination . I have concerns.  ,
LINC01278 Sponges miR‚Ä?00b‚Ä?p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection
Authors: Zhicheng Zhu
Yong Wang
Kexiang Liu
Weitie Wang
Dan Li
Tiance Wang
Qing Liu
Hulin Piao
Journal: Journal of the American Heart Association (2021)
Discipline: CLINICAL MEDICINE
Keywords: ACTG2; aortic dissection; gene profiling; linc01278; miR‚Ä?00b‚Ä?p
Affiliations: Department of Cardiovascular Surgery of the Second Hospital of Jilin University Changchun Jilin China, Graduate School of Medicine and Faculty of Medicine of the University of Tokyo Tokyo Japan

Abstract:  Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. We integrated the mRNA microarray data set with GSE52093 to determine the differentially expressed genes. Bioinformatic analysis, including Gene Expression Omnibus 2R, Venn diagram analysis, gene ontology, pathway enrichment, and protein-protein interaction networks were used to identify the target lncRNA, microRNA, and mRNA involved in AD. Subsequently, we validated the bioinformatics data using techniques in molecular biology in human tissues and VSMCs. Linc01278, microRNA-500b-5p, and ACTG2 played an important role in the vascular smooth muscle contraction pathway. Linc01278 and ACTG2 were downregulated and miR-500b-5p was upregulated in AD tissues. Molecular markers of VSMC phenotypic switching, including SM22Œ±, SMA, calponin, and MYH11, were downregulated in AD tissues. Plasmid-based overexpression and RNA interference-mediated downregulation of linc01278 weakened and enhanced VSMC proliferation and phenotypic switching, respectively. Dual-luciferase reporter assays confirmed that linc01278 regulated miR-500b-5p that directly targeted ACTG2 in HEK293T cells. Conclusions These data demonstrate that linc01278 regulates ACTG2 to control the phenotypic switch in VSMCs by sponging miR-500b-5p. This linc01278-miR-500b-5p-ACTG2 axis has a potential role in developing diagnostic markers and therapeutic targets for AD. 

Retracted: No

PubPeer comments:
 Fig.12 (f), row beta-actin, rendered doubtful 1. looped parts were peculiarly brighter to pure white that cannot be explained by inadequate membrane cutting, poor blocking, excessive ECL fluid or uneven electrophoresis, though the upper part looked usual. 2. unnatural blot stain-blank transition on 4th column lower part 3. confusing halos appeared at the blots upper part.  ,
Environmentally durable superhydrophobic surfaces with robust photocatalytic self-cleaning and self-healing properties prepared via versatile film deposition methods
Authors: Tao Wang
Robert S Gurney
Dan Liu
Zhiwei Huang
Journal: Journal of Colloid and Interface Science (2018)
Discipline: CHEMISTRY
Keywords: Photocatalytic; Self-cleaning; Self-healing; Superhydrophobic.
Affiliations: School of Materials Science and Engineering, Wuhan University of Technology, Wuhan 430070, China., School of Materials Science and Engineering, Wuhan University of Technology, Wuhan 430070, China. Electronic address: .

Abstract:  Superhydrophobic (SH) surfaces with self-cleaning photocatalytic properties have become an important research focus in recent years. In this work, we fabricated multifunctional and environmentally durable SH surfaces via a facile one-step reaction of octadecyl isocyanate (ODI) with TiO2 particles. The resulting films possess SH properties, facilitated by a combination of hydrophobic long alkyl chains and the hierarchical crystalline structure. Films can be prepared via spray or blade coating on a variety of hard and soft substrates, and function well when exposed to either air or oil. The coating retains its SH properties for at least 6 months in ambient conditions, and after organic pollution it can recover its SH properties using UV or sun light illumination. After water impalement, the SH properties can self-heal via the self-assembly of long alkyl chains to their original state within several hours at ambient conditions, or within minutes on a heating stage. The covalent bonds between alkyl chains and TiO2, together with hydrogen bonds between adjacent alkyl chains, greatly increased the surface durability of the SH films. This multifunctional SH coating is a very promising material for commercial and industrial coating applications. 

Retracted: No

PubPeer comments:
 Reference [36]: This article is nothing to do with coating, and there is no one called Lu. among the authors. What is the correct reference? ,
Critical role for lipid raft-associated Src kinases in activation of PI3K-Akt signalling
Authors: Teresa D Tetley
Anne G Bittermann
Umme K Khanzada
Margaret C Frame
Maria E Espinosa del Hierro
Alexandre Arcaro
Muriel Aubert
Michael J Seckl
Smaragda Angelidou
Journal: Cellular Signalling (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Lipid rafts; growth factor receptors; PI3K signalling; Src; protein kinase B (PKB)/Akt
Affiliations: Lung Cancer Biology Group, Division of Medicine, Imperial College Faculty of Medicine, Hammersmith Hospital Campus, Du Cane Road, London W12 ONN, United Kingdom. 

Abstract:  Lipid rafts are membrane microdomains distinct from caveolae, whose functions in polypeptide growth factor signalling remain unclear. Here we show that in small cell lung cancer (SCLC) cells, specific growth factor receptors such as c-Kit associate with lipid rafts and that these domains play a critical role in the activation of phosphoinositide 3-kinase (PI3K) signalling. The class IA p85/p110alpha associated with Src in lipid rafts and was activated by Src in vitro. Lipid raft integrity was essential for Src activation in response to stem cell factor (SCF) and raft disruption selectively inhibited activation of protein kinase B (PKB)/Akt in response to SCF stimulation. Moreover, inhibition of Src kinases blocked PKB/Akt activation and SCLC cell growth. The use of fibroblasts with targeted deletion of the Src family kinase genes confirmed the role of Src kinases in PKB/Akt activation by growth factor receptors. Moreover a constitutively activated mutant of Src also stimulated PI3K/Akt in lipid rafts, indicating that these microdomains play a role in oncogenic signalling. Together our data demonstrate that lipid rafts play a key role in the activation of PI3K signalling by facilitating the interaction of Src with specific PI3K isoforms. 

Retracted: No

PubPeer comments:
 On page 1276,  The optimized Bi films with a thickness of 250 nm were lithographically patterned in the conventional Hall geometry as shown in Figure 1a and Figure 2a with an active area of the Hall sensor of 100 u03bcm u00d7 100 u03bcm. But Figure 2a shows a 230nm thickness Bi film. why the active area is 100 u03bcm u00d7 100 u03bcm? Isn t it a cross? ,
External Qi of Yan Xin Qigong induces cell death and gene expression alterations promoting apoptosis and inhibiting proliferation, migration and glucose metabolism in small-cell lung cancer cells
Authors: Igor Dozmorov
Wei Cao
Feng Li
Ming Dao
Michael Centola
Xin Yan
Dan Hu
Mark Barton Frank
Journal: Molecular and Cellular Biochemistry (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Small-cell lung cancer; Yan Xin Qigong; External Qi; apoptosis; gene expression profiling
Affiliations: The Institute of Chongqing Traditional Chinese Medicine, Chongqing, China.

Abstract:  Small-cell lung cancer (SCLC) is a highly malignant carcinoma with poor long-term survival. Effective treatment remains highly demanded. In the present study, we demonstrated that External Qi of Yan Xin Qigong (YXQ-EQ) exerted potent cytotoxic effect towards SCLC cell line NCI-H82 via induction of apoptosis. Global gene expression profiling identified 39 genes whose expression was altered by YXQ-EQ in NCI-82 cells. Among them, semi-quantitative RT-PCR and real-time qPCR analyses confirmed that the gene expression levels of apoptotic proteins death-associated protein kinase 2 and cell death-inducing DFFA-like effector b were upregulated, whereas that of oncoproteins DEK and MYCL1, cell migration-promoting proteins CD24 and integrin-alpha 9, and glycolytic enzyme aldolase A were downregulated. These findings suggest that YXQ-EQ may exert anticancer effect through modulating gene expression in a way that facilitates cancer cell apoptosis while represses proliferation, metastasis, and glucose metabolism. 

Retracted: No

PubPeer comments:
 Immunoblotting of Actin in Figure 1A was reappeared in another paper published by the same team (DOI: 10.1038 sj.onc.1205896). See figure below.  , 
 #1 Dear Cicindela Chrysippe, Thank you for your interest of our study and we appreciate your comments. By carefully checking our original data, we confirm that there was no problem in this study. Regrettably, there was a mistake by copy error in the mentioned paper (another paper published by our team (DOI: 10.1038 sj.onc.1205896), and we have sent an erratum to the editor office of the journal. Many thanks for your comment again. ,
Nitric oxide induces hypoxia-inducible factor 1 activation that is dependent on MAPK and phosphatidylinositol 3-kinase signaling
Authors: Gregg L Semenza
Shinae Kizaka-Kondoh
Junji Yodoi
Takehiko Adachi
Kazuhiko Fukuda
Kiichi Hirota
Satoshi Takabuchi
Kenji Kasuno
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hypoxia-inducible factor-1 (HIF-1); NO donor; HIF-1alpha expression; Transcriptional activity; Protein synthesis
Affiliations: Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, IKEDA, Osaka, Japan 563-0053.

Abstract:  Hypoxia-inducible factor-1 (HIF-1) is a master regulator of cellular adaptive responses to hypoxia. Levels of the HIF-1alpha subunit increase under hypoxic conditions. Exposure of cells to certain nitric oxide (NO) donors also induces HIF-1alpha expression under nonhypoxic conditions. We demonstrate that exposure of cells to the NO donor NOC18 or S-nitrosoglutathione induces HIF-1alpha expression and transcriptional activity. In contrast to hypoxia, NOC18 did not inhibit HIF-1alpha hydroxylation, ubiquitination, and degradation, indicating an effect on HIF-1alpha protein synthesis that was confirmed by pulse labeling studies. NOC18 stimulation of HIF-1alpha protein and HIF-1-dependent gene expression was blocked by treating cells with an inhibitor of the phosphatidylinositol 3-kinase or MAPK-signaling pathway. These inhibitors also blocked NOC18-induced phosphorylation of the translational regulatory proteins 4E-BP1, p70 S6 kinase, and eIF-4E, thus providing a mechanism for the modulation of HIF-1alpha protein synthesis. In addition, expression of a dominant-negative form of Ras significantly suppressed HIF-1 activation by NOC18. We conclude that the NO donor NOC18 induces HIF-1alpha synthesis under conditions of NO formation during normoxia and that hydroxylation of HIF-1alpha is not regulated by NOC18. 

Retracted: No

PubPeer comments:
 Figures 1A and 8B. Much more similar and different than expected.  , 
 Figure 9B. Much more similar than expected after horizontal flip.  , 
 And in Fig. 10, there is reuse of an immunoblot gel slice, shifted by two lanes and labelled as two different proteins. Does not compute.  There is also a horizontally flipped gel slice in Fig. 10 that could do with being marked up as time permits. , 
 As mentioned above, in Fig. 10, there is also a reused and horizontally flipped immunoblot gel slice. Enjoy!  ,
Killing of lymphoblastic leukemia cells by nitric oxide and taxol: involvement of NF-Œ∫B activity
Authors: M C Santos-Silva
M Sampaio de Freitas
J Assreuy
Journal: Cancer Letters (2001)
Discipline: CLINICAL MEDICINE
Keywords: Nitric oxide; Taxol; NF-kappaB; Cytotoxicity; Leukemia cells

Abstract:  Nitric oxide (NO) and taxol are cytotoxic towards leukemia and tumor cells and interfere with the transcription factor NF-kappaB activity. NO and taxol inhibited NF-kappaB activity and were cytotoxic to human and murine leukemia cells, but at a different magnitude (30% cell killing and 80% inhibition of NF-kappaB). Sub-effective concentrations of SNAP and taxol synergized in killing L-1210 cells but either alone or in combination completely inhibited NF-kappaB. Pyrrolidine dithiocarbamate (PDTC) was cytotoxic on its own and inhibited NF-kappaB activity. It potentiated NO and taxol killing but again there was no direct relationship between inhibition of NF-kappaB and cell killing. Neither NO nor taxol cytotoxicity was related to the cytoskeleton. Our results show that NO, taxol and PDTC induced apoptosis and NF-kappaB inhibition in leukemic cells but their cytotoxicity either alone or in combination, does not seem to be dependent on the inhibition of NF-KB activity. 

Retracted: No

PubPeer comments:
 Figures 3 and 4: * Some bands appear to be visible multiple times while representing different conditions.  The same bands also appear in other papers by the same first author, i.e. DOI 10.1016 j.leukres.2005.06.021 https: pubpeer.com publications 48BB2206B3F176830827EBB89346C5 and 10.1016 S0925-4439(03)00096-6 https: pubpeer.com publications B7E253C7712EA443A96BD248B5C95D They are also visible in the constellation of this paper in MC Santos da Silva s PhD thesis found here: https: repositorio.ufsc.br bitstream handle 123456789 84103 183506.pdf ,
Preventing oxidative stress: a new role for XBP1
Authors: T A Rando
S Zhao
M Hareyama
Dan Luo
K Imai
M Adachi
Y Liu
A C Koong
Y Shinomura
Journal: Cell death and differentiation (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Antioxidant molecules; oxidative stress; reactive oxygen species (ROS); X-box-binding protein (XBP1); endoplasmic reticulum stress
Affiliations: Division of Molecular Oncology and Molecular Diagnosis, Sapporo Medical University School of Medicine, Chuo-Ku, Sapporo, Japan.

Abstract:  Antioxidant molecules reduce oxidative stress and protect cells from reactive oxygen species (ROS)-mediated cellular damage and probably the development of cancer. We have investigated the contribution of X-box-binding protein (XBP1), a major endoplasmic reticulum stress-linked transcriptional factor, to cellular resistance to oxidative stress. After exposure to hydrogen peroxide (H(2)O(2)) or a strong ROS inducer parthenolide, loss of mitochondrial membrane potential (MMP) and subsequent cell death occurred more extensively in XBP1-deficient cells than wild-type mouse embryonic fibroblast cells, whereas two other anticancer agents induced death similarly in both cells. In XBP1-deficient cells, H(2)O(2) exposure induced more extensive ROS generation and prolonged p38 phosphorylation, and expression of several antioxidant molecules including catalase was lower. Knockdown of XBP1 decreased catalase expression, enhanced ROS generation and MMP loss after H(2)O(2) exposure, but extrinsic catalase supply rescued them. Overexpression of XBP1 recovered catalase expression in XBP1-deficient cells and diminished ROS generation after H(2)O(2) exposure. Mutation analysis of the catalase promoter region suggests a pivotal role of CCAAT boxes, NF-Y-binding sites, for the XBP1-mediated enhancing effect. Taken together, these results indicate a protective role of XBP1 against oxidative stress, and its positive regulation of catalase expression may at least in part account for this function. 

Retracted: No

PubPeer comments:
  , 
 #1 This seems to be an an obvious problem. What would be the reason for the authors to choose not to address this? *** Inverse  ,
MicroRNA-1179 suppresses the proliferation and enhances vincristine sensitivity of oral cancer cells via induction of apoptosis and modulation of MEK/ERK and PI3K/AKT signalling pathways
Authors: Yanmei Gao
Tiemin Pu
Hanmei Xu
Journal: AMB Express (2020)
Discipline: MICROBIOLOGY
Keywords: Autophagy; Metastasis; Micro RNA; Oral cancer; Proliferation.
Affiliations: Department of Stomatology, Affiliated Hospital of Jilin Medical University, NO 81 of Road Huashan, Fengman Area, Jilin, 132013, China., Department of Stomatology, Affiliated Hospital of Jilin Medical University, NO 81 of Road Huashan, Fengman Area, Jilin, 132013, China. .

Abstract:  The role of miR-1179 in the development of cancer has been proved by different studies. However, the expression profile and role of miR-1179 is yet to be explored in human oral cancer. Consistently, this study was undertaken to explore the molecular role of miR-1179 in regulation of the human oral cancer development and progression. The results showed miR-1179 to be significantly (p &lt; 0.05) overexpressed in all the oral cancer cell lines relative to normal cells. The repression of miR-1179 transcript levels not only suppressed the proliferation of oral cancer cells but also increased their sensitivity to vincristine. The decline in proliferative rates was attributed to induction of autophagy in oral cancer cells as confirmed by transmission electron microscopic analysis. Western blot analysis showed that the expression of LC3B-II increased and that of beclin 1 decreased while LC3B-I expression remained constant upon miR-1179 inhibition. Inhibition of miR-1179 caused significant decrease in the migration and invasion of the oral cancer cells. The migration and invasion found to be 47% and 32% for SCC-9 and 24% and 28% for SCC-25 cells upon miR-1179 inhibition. At molecular level, the miR-1179 was shown to exert its anticancer effects via deactivation of MEK/ERK and PI3K/AKT signalling cascades. In conclusion, the findings point towards the potential of miR-1179 in the treatment of oral cancer. 

Retracted: No

PubPeer comments:
 *[left]* Fig 5.  Inhibition of miR-1179 blocks MEK ERK and PI3K and AKT signalling pathways. a Western blots showing the effects of miR-1179 inhibition on expression of MEK, p-MEK, ERK and p-ERK proteins in SCC-9 and SCC-25 cells. b Western blots showing the effects of miR-1179 inhibition on expression of PI3K, p-PI3K, AKT and p-AKT proteins in SCC-9 and SCC-25. *[upper right]* Fig 5 from [Tang et al (2020)] .  Western blotting assay indicating the expressions of MEK ERK signalling pathway associated proteins. *[lower right]* Figure 8 from [Xu et al (2020)] .  Western blot analysis showing the effect of Shionone on the MEK ERK and STAT3 signalling pathway in SK-BR-3 cells. The Figure shows that the expression of p-ERK, p-MEK and p-STAT-3 decreases in a dose-dependent manner upon Shionone treatment .  Other manifestations of the versatile loading control are linked [here] . ,
DNA content as a prognostic marker in patients with oral leukoplakia
Authors: W Kildal
H S Koppang
J Sudb√∏
A Reith
B Risberg
H E Danielsen
Journal: New England Journal of Medicine (2001)
Discipline: CLINICAL MEDICINE
Keywords: Oral leukoplakia; squamous-cell carcinoma; DNA ploidy; histologic grade; disease-free survival
Affiliations: Department of Pathology, Norwegian Radium Hospital and University of Oslo. 

Abstract:  Background: Oral leukoplakia may develop into squamous-cell carcinoma, which has a poor prognosis. Risk factors for oral carcinoma have been identified, but there are no reliable predictors of the outcome in individual patients with oral leukoplakia. Methods: We identified 150 patients with oral leukoplakia that was classified as epithelial dysplasia and measured the nuclear DNA content (ploidy) of the lesions to determine whether DNA ploidy could be used to predict the clinical outcome. Biopsy specimens obtained at annual follow-up visits were graded histologically and classified with respect to DNA content in a blinded fashion. Disease-free survival was assessed in relation to DNA ploidy and the histologic grade. The mean duration of follow-up was 103 months (range, 4 to 165). Results: Among 150 patients with verified epithelial dysplasia, a carcinoma developed in 36 (24 percent). Of the 150 patients, 105 (70 percent) had diploid (normal) lesions, 20 (13 percent) had tetraploid (intermediate) lesions, and 25 (17 percent) had aneuploid (abnormal) lesions at the time of the initial diagnosis. A carcinoma developed in 3 of the 105 patients with diploid lesions (3 percent), as compared with 21 of the 25 patients with aneuploid lesions (84 percent), yielding a negative predictive value of 97 percent with respect to the diploid lesions and a positive predictive value of 84 percent with respect to the aneuploid lesions. Carcinoma developed in 12 of 20 patients with tetraploid lesions (60 percent). The mean time from the initial assessment of the DNA content to the development of a carcinoma was 35 months (range, 4 to 57) in the group with aneuploid lesions and 49 months (range, 8 to 78) in the group with tetraploid lesions (P=0.02). The cumulative disease-free survival rate was 97 percent among the group with diploid lesions, 40 percent among the group with tetraploid lesions, and 16 percent among the group with aneuploid lesions (P&lt;0.001). Conclusions: The DNA content in cells of oral leukoplakia can be used to predict the risk of oral carcinoma. 

Retracted: Yes

PubPeer comments:
 This article got retracted in 2006, together with a 2004 paper by the same researchers. The retraction notice can be found here: https: www.nejm.org doi full 10.1056 NEJMe068247 In an earlier 2004 Expression of Concern (found here: https: www.nejm.org doi full 10.1056 NEJMe068020 ), it was stated that  Figures 3B and 3C of that article, which purport to represent two different patients and stages of oral epithelial dysplasia, are in fact different magnifications of the same photomicrograph. Here is Figure 3, with a rather obvious duplicated area marked with blue boxes.  ,
Vaginal cleansing prior to caesarian section: To do or not to do?: A randomized trial
Authors: Nisreen Khaled Aref
Journal: Journal of Gynecology Obstetrics and Human Reproduction (2019)
Discipline: CLINICAL MEDICINE
Keywords: Cesarean section; Infectious morbidity; Povidone iodine.
Affiliations: Faculty of Medicine, Taif University, Saudi Arabia. Electronic address: .

Abstract:  Purpose: To evaluate the efficacy of preoperative vaginal cleansing using povidone-iodine solution 10% on rates of post cesarean section (CS) infectious morbidities (endometritis, febrile morbidity and wound infection). Methods: This prospective randomized trial was conducted among 226 pregnant women scheduled for term elective CS. Patients were equally divided into two groups by simple randomization method. The study group had preoperative vaginal cleansing using povidone-iodine solution 10% for about 1 min, while the control group did not. All cases received the prophylactic antibiotics and the usual abdominal scrub. Adverse post CS infectious morbidities such as endometritis, febrile morbidity and wound infection were observed at the time of hospital discharge and weekly for 6 weeks postpartum. Results: Both groups were matched regarding the baseline patients' characteristics. Overall, post-CS infectious morbidity was significantly reduced from 20.7% in the control group to 7.5% in the intervention group. Marked significant reduction was seen in the incidence of endometritis (11.8% in the control group versus 2.8% in the intervention group). However, maternal fever and wound infection showed no significant difference between both groups. Conclusion: Vaginal cleansing with povidone-iodine solution 10% prior to elective CS appears to be effective in reducing rates of post-CS infectious morbidity mainly endometritis. 

Retracted: No

PubPeer comments:
 The XRD spectra in the figure below contain stretches of duplicated data. Is this problem possibly similar to https: pubpeer.com publications 06AF3B4083FF664876042C55F9DFA7#2 and https: pubpeer.com publications CD61236B5BF3D92E326064FB8BA6BC#1?  [ click to animate, black curve turns red ]  ,
Regulation of urokinase production by androgens in human prostate cancer cells: effect on tumor growth and metastases in vivo
Authors: S A Rabbani
R H Xing
Journal: Endocrinology (1999)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: prostate cancer; urokinase; androgens; AR; PC-3 cells
Affiliations: Department of Medicine, McGill University and Royal Victoria Hospital, Montr√©al, Qu√©bec, Canada., Departments of Medicine, Physiology and Oncology, McGill University and Royal Victoria Hospital, MontreÃÅal, QueÃÅbec Canada, H3A 1A1

Abstract:  During the complex multistep process of tumor progression, prostate cancer is initiated as an androgen-sensitive, nonmetastatic cancer, followed by a gradual transition into a highly metastatic and androgen-insensitive variety that lacks the expression of functional androgen receptors (AR). Urokinase (uPA), a member of the serine protease family, has been implicated in the progression of various human malignancies, including prostate cancer. Although uPA production is regulated by various growth factors and cytokines, the role of sex steroids (androgens) in regulating uPA gene expression in prostate cancer is poorly understood. In the current study, we have examined the role of androgens in regulating uPA production and the invasive capacity of the androgen insensitive PC-3 cells transfected with the full-length human AR complementary DNA (PC-3T). Restoration of androgen responsiveness in PC-3T cells caused a marked decrease in cell doubling time. Treatment of PC-3T cells with dihydroxytestosterone (DHT) caused a dose-dependent decrease in uPA messenger RNA and protein production, resulting in their decreased ability to invade through the Matrigel. Nuclear runoff assays revealed that these effects were attributable to the ability of DHT to inhibit uPA gene transcription. AR antagonist flutamide (Flu) reversed the effect of DHT on proliferation and invasion of PC-3T cells. Both control (PC-3) and experimental (PC-3T) cells were injected into the right flank of male BALB/c nu/nu mice. Control animals developed palpable tumors and microscopic tumor metastases at lymph nodes, lungs, and liver at 6-week posttumor cell inoculation. In contrast to this, because of androgen sensitivity of PC-3T cells, palpable tumors were observed only at week 12, with occasional tumor metastases in lungs. Furthermore, inoculation of PC-3T cells into surgically castrated host animals resulted in the development of tumors at a much earlier time (week 10) and a high incidence of metastases, compared with regular animals receiving PC-3T cells. Collectively, these results demonstrate the ability of androgen to regulate uPA production, which may directly effect prostate cancer growth, invasion, and metastasis in vitro and in vivo. 

Retracted: No

PubPeer comments:
 Figure 5. Much more similar than expected.  ,
Correlation Between IL-20 and De Quervain's Disease Severity
Authors: Yao-Lung Kuo
Che-Chia Hsu
Ping-Hui Wang
I-Ming Jou
Tai-Hua Yang
Ching-Ju Shen
Journal: Annals of Plastic Surgery (2019)
Discipline: CLINICAL MEDICINE
Keywords: De Quervain's disease; stenosing tenosynovitis; first dorsal compartment; wrist; histopathological studies
Affiliations: Department of Orthopedics, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan., Department of Orthopedics, Chi-Mei Medical Center, Tainan, Taiwan., Department of Orthopedics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan., Department of Gynecology and Obstetrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.

Abstract:  De Quervain's disease is a stenosing tenosynovitis of the first dorsal compartment of the wrist. Histopathological studies have reported that the thickening of the first dorsal retinaculum is characterized by degeneration rather than inflammation. However, significant infiltration of mast cells and macrophages was noted in a torn tendon study, which suggested that innate immune pathways are part of the mechanism that mediates early tendinopathy. Recently, Interleukin-20 (IL-20) has been reported to provoke potent inflammation and regulate angiogenesis and chemotaxis, which are important for the pathogenesis of inflammatory diseases. The main purpose of our study was to investigate the correlation between IL-20 and tumor necrosis factor (TNF-Œ±) and clarify the potential predictor of tendinopathy progression. Hematoxylin and eosin (H &amp; E) and immunohistochemistry (IHC) staining were used to score and analyze the clinical outcome. TNF-Œ±, IL-20 and related inflammation cytokines were examined. Moreover, the tenocytes were cultured with a stimulator and were used to examine inflammatory cytokine secretions. A real-time polymerase chain reaction (Real-time PCR) was used to detect the gene expression profile. The IHC data showed that TNF-Œ± is up-regulated in grade III de Quervain's. The analysis data showed that IL-20 is positively correlated with TNF-Œ± and disease severity. The real-time PCR showed that the inflammation stimulator enhanced the expression of IL-20 mRNA expression. Inflammation cytokines such as TNF-alpha, transforming growth factor-Œ≤ (TGF-Œ≤) and IL-1 have been used as predictors of de Quervain's; IL-20 is a new predictor based on this study. In the future, IL-20 expression's involvement in the molecular mechanism of the severity of de Quervain's should be further investigated. 

Retracted: No

PubPeer comments:
 Three Raman spectroscopy in **Figure 1** from this article is the same with **Figure 2** in **https: iopscience.iop.org article 10.7567 1347-4065 aafe70**.  SEM from **Figure 1 (700 C)** in this article is also the same with **Figure 2e** in **https: iopscience.iop.org article 10.7567 1347-4065 aafe70**.  Can the authors confirm this? ,