PReD-Bench/PRed-Bench huggingface dataset:
B10 cells decrease fibrosis progression following cardiac injury partially by IL‐10 production and regulating hyaluronan secretion
Authors: Fang Liu
Shiqing Zhang
Zhaoliang Su
Rong Chen
Huaxi Xu
Yu Tian
Yuwen Cao
Nan Che
Lin Xia
Journal: Journal of Leukocyte Biology (2021)
Discipline: IMMUNOLOGY
Keywords: B10 cells; HA; Mϕ; cardiac injury.
Affiliations: International Genome Center Jiangsu University  Zhenjiang China, Department of Rheumatology The First affiliated Hospital of Nanjing Medical University  Nanjing China, Department of Immunology, School of Medicine Jiangsu University  Zhenjiang China

Abstract:  B10 cells play negative roles in inflammatory disorders by producing IL-10. However, their effects on fibrosis have not been elucidated. Therefore, this study was conducted to examine the dynamic changes of B10 cell frequency and their potential role in cardiac fibrosis. We found that the frequency of B10 cells was significantly increased, and they participated in the regression of fibrosis via IL-10, particularly by accelerating hyaluronan secretion and inhibiting collagen deposition. In vivo, hyaluronan ablation or treatment significantly restricted cardiac fibrosis development. hyaluronan-induced conversion of M1/M2 Mc was dependent on the size of hyaluronan. Low molecular weight hyaluronan promoted the conversion to M1 Mϕ, whereas medium and high molecular weight hyaluronan accelerated Mϕ transdifferentiation into the M2 phenotype. Adoptive transfer of B10 cells significantly attenuated collagen deposition whereas CD19-/- mice with reduced B10 cells exacerbated fibrosis following cardiac injury. Our results provide new evidence suggesting that B10 cells exert antifibrotic effects by regulating the extracellular matrix composition during cardiac injury, and also highlight that B10 cells may serve as a promising therapeutic candidate for managing cardiac fibrosis-associated disorders. 

Retracted: No

PubPeer comments:
 Fig. 2E has an overlap between 2 images with subtle difference in brightness contrast. Can the authors provide an explanation? ![file] , 
 #1 Dear Tulipa Thanks for your raising the problems. we had checked the original records. we truly made a mistake. the two images are truly from the same sample. we apply to correct. however, there is oh, the conclusion is reliable. I hope you can give us more comments for our work. best wishes ![file] ,
Lactate: the ugly duckling of energy metabolism
Authors: Sven Enerbäck
Joshua D Rabinowitz
Journal: Nature Metabolism (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Lactate; Metabolic waste product; Fermentation products; ATP; Oxygen
Affiliations: Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA. ., Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden. .

Abstract:  Lactate, perhaps the best-known metabolic waste product, was first isolated from sour milk, in which it is produced by lactobacilli. Whereas microbes also generate other fermentation products, such as ethanol or acetone, lactate dominates in mammals. Lactate production increases when the demand for ATP and oxygen exceeds supply, as occurs during intense exercise and ischaemia. The build-up of lactate in stressed muscle and ischaemic tissues has established lactate's reputation as a deleterious waste product. In this Perspective, we summarize emerging evidence that, in mammals, lactate also serves as a major circulating carbohydrate fuel. By providing mammalian cells with both a convenient source and sink for three-carbon compounds, circulating lactate enables the uncoupling of carbohydrate-driven mitochondrial energy generation from glycolysis. Lactate and pyruvate together serve as a circulating redox buffer that equilibrates the NADH/NAD ratio across cells and tissues. This reconceptualization of lactate as a fuel-analogous to how Hans Christian Andersen's ugly duckling is actually a beautiful swan-has the potential to reshape the field of energy metabolism. 

Retracted: No

PubPeer comments:
 A discussion of the inherent difficulties in measuring the rate of lactate production using isotope infusions would seem appropriate when dealing with this topic. These issues have been known for decades but seem to have been largely forgotten. The implications are significant for this field and worth reminding people of. Example of some key references: Robert R. Wolfe (1990) Isotopic Measurement of Glucose and Lactate Kinetics, Annals of Medicine, 22:3, 163-170, DOI: 10.3109 07853899009147263 Wolfe RR, Jahoor F, Miyoshi H. Evaluation of the isotopic equilibration between lactate and pyruvate. Am J Physiol. 1988;254(4 Pt 1):E532-E535. doi:10.1152 ajpendo.1988.254.4.E532 J. A. Romijn et al., Lactate-pyruvate interconversion in blood: implications for in vivo tracer studies American Journal of Physiology - Endocrinology and Metabolism, 1994 Sahlin K. Lactate production cannot be measured with tracer techniques. Am J Physiol. 1987;252(3 Pt 1):E439-E440. doi:10.1152 ajpendo.1987.252.3.E439 , 
 This paper also deals with this issue: Xiao-junZhang, Hidefumi Baba, Robert R.Wolfe. Further evaluation of isotopic equilibration between labeled pyruvate and lactate. The Journal of Nutritional Biochemistry Volume 4, Issue 4, April 1993, Pages 218-221 ,
Combining use of Phillyrin and autophagy blocker alleviates laryngeal squamous cell carcinoma via AMPK/mTOR/p70S6K signaling
Authors: Xi He
Qing He
Da-Hua Wang
Journal: Bioscience reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 3-methyladenine; Phillyrin; autophagy; chloroquine; laryngeal squamous cell carcinoma.
Affiliations: Department of Otolaryngology, Xuzhou Municipal Hospital Affiliated with Xuzhou Medical University, Xuzhou 221002, China ., Department of Dermatology, Xuzhou Municipal Hospital Affiliated with Xuzhou Medical University, Xuzhou 221002, China., Department of Neurology, Xuzhou Municipal Hospital Affiliated with Xuzhou Medical University, Xuzhou 221002, China.

Abstract:  Phillyrin (PHN), one of the major active constituents of Forsythia suspensa and F. koreana, has been reported to produce antioxidant, antibacterial, anti-obesity and anti-inflammatory effects. However, no study has demonstrated the role of PHN in laryngeal squamous cell carcinoma (LSCC). We aimed to investigate the effects of PHN on the proliferation and apoptosis of HEp-2 cells. In the present study, PHN alone showed little effect on HEp-2 cell proliferation and apoptosis. Subsequent tests showed that PHN could largely enhance the level of autophagy on HEp-2 cells. Combining use of PHN and autophagy blockers including 3-methyladenine (3-MA) and chloroquine (CQ) significantly inhibited HEp-2 cell proliferation in a dose- and time-dependent manner and induced apoptosis after 24 h in a dose-dependent manner. Additionally, we found that the possible underlying molecular mechanism of PHN-induced autophagy might be through the AMPK/mTOR/p70S6K signaling pathway. Taken together, our study indicates that combining use of PHN and autophagy blockers may serve as a novel strategy in LSCC treatment. 

Retracted: No

PubPeer comments:
 The Western blot in figure 6D may show signs of a splice, and two smears look unexpectedly similar, with different focus. Could the authors please supply the uncropped original scan? *** Enhanced contrast ![file] *** Original contrast ![file] *** Full figure ![file] ,
Retracted : Long noncoding RNA PCA3 regulates prostate cancer through sponging miR‐218‐5p and modulating high mobility group box 1
Authors: Chuanchuan Ren
Xiangfei He
Guoxian Zhang
Juntang Lin
Qingwei Wang
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: high mobility group box 1 (HMGB1); long noncoding RNA (lncRNA) prostate cancer antigen 3 (PCA3); miR-218-5p; prostate cancer.
Affiliations: Department of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China., Key-Disciplines Laboratory Clinical-Medicine Henan, Zhengzhou, Henan, China., Stem Cell and Biotherapy Research Center of Xinxiang Medical University, Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang, Henan, China.

Abstract:  Objective: The purpose of this study was to investigate the mechanism of long noncoding RNA (lncRNA) prostate cancer antigen 3 (PCA3) in prostate cancer (PCa) via regulating the miR-218-5p/high mobility group box 1 (HMGB1) axis. Methods: The Cancer Genome Atlas database was used to divide differentially expressed lncRNAs, microRNAs, and messenger RNA (mRNAs). The mRNA expressions of lncRNA PCA3, miR-218-5p, and HMGB1 were determined by reverse transcription polymerase chain reaction. Cell propagation was evaluated using the Cell Counting Kit-8 assay and the apoptotic rate was examined by flow cytometry. Cell migration and invasion were observed through the wound healing assay and transwell assay. Target relationships among PCA3, miR-218-5p, and HMGB1 were validated via dual-luciferase reporter gene assay. A nude mouse model in vivo was designed to evaluate the effect of PCA3 on prostate tumor growth. Results: PCA3 and HMGB1 were high-expressed in PCa, whereas miR-218-5p was low-expressed. PCA3 knockdown or miR-218-5p overexpression suppressed PCa cell proliferation, migration, and invasion, but promoted apoptosis. Besides, targeted relationships and interactions on the expression between miR-218-5p and PCA3 or HMGB1 were elucidated. PCA3 weakened cell viability and mobility whereas induced apoptosis through binding with miR-218-5p. Meanwhile, miR-218-5p also inhibited PCa tumorigenesis via downregulation of HMGB1. Knockdown of PCA3 impeded tumor growth by downregulating its downstream gene HMGB1. Conclusions: lncRNA PCA3 facilitated PCa progression through sponging miR-218-5p and regulating HMGB1. 

Retracted: Yes

PubPeer comments:
 Retracted [20 July 2021] . ---------------------------------------------- The above article, published online on 19 December 2018 in Wiley Online Library , has been retracted by agreement between the journal s Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found. Thus, the editors consider the conclusions of this article to be invalid. ----------------------------- Not previously flagged on Pubpeer. ,
Regulation of the Fanconi anemia group C protein through proteolytic modification
Authors: Georges Lévesque
Isabelle Goulet
Caroline Huard
Chantal Godin
Marie-Chantal Delisle
Manuel Buchwald
Isabelle Brodeur
Cédric S Tremblay
Edward W Khandjian
Madeleine Carreau
Chantal Charbonneau
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Fanconi anemia group C protein; FANCC; damage response signaling; cytoplasm; messenger
Affiliations: Unité de Génétique Humaine et Moléculaire, CHUQ-Pavillon St-François d'Assise, Quebec, Quebec G1L 3L5, Canada.

Abstract:  The function of the Fanconi anemia group C protein (FANCC) is still unknown, though many studies point to a role in damage response signaling. Unlike other known FA proteins, FANCC is mainly localized to the cytoplasm and is thought to act as a messenger of cellular damage rather than an effector of repair. FANCC has been shown to interact with several cytoplasmic and nuclear proteins and to delay the onset of apoptosis through redox regulation of GSTP1. We investigated the fate and function of FANCC during apoptosis. Here we show that FANCC undergoes proteolytic modification by a caspase into a predominant 47-kDa ubiquitinated protein fragment. Lack of proteolytic modification at the putative cleavage site delays apoptosis but does not affect MMC complementation. These results suggest that FANCC function is regulated through proteolytic processing. 

Retracted: No

PubPeer comments:
 ![file] ,
Highly selective and sensitive fluorescence sensing of nanomolar Zn ions in aqueous medium using Calix[4]arene passivated Carbon Quantum Dots based on fluorescence enhancement: Real-time monitoring and intracellular investigation
Authors: Hemant Sharma
Navneet Kaur
Pushap Raj
Harpreet Kaur
Narinder Singh
Meenakshi Verma
Journal: Analytica chimica acta (2018)
Discipline: CHEMISTRY
Keywords: Calix [4] arene; Carbon quantum dots (CDs); Fluorescence spectroscopy; Sensor; Surface functionalization.
Affiliations: Centre for Nanoscience and Nanotechnology, Panjab University, Chandigarh, 160014, India., Department of Chemistry, IIT Ropar, Roopnagar, Punjab, 140001, India., Department of Chemistry, IIT Ropar, Roopnagar, Punjab, 140001, India. Electronic address: ., Department of Chemistry, Panjab University, Chandigarh, 160014, India. Electronic address: .

Abstract:  Carbon Quantum Dots (CDs) owing to its unique photophysical properties have attracted immense consideration of the researchers in last decade to explore its applications in the fields of bio-imaging and sensing. In the present work, we have developed a novel CDs functionalized with Calix[4]arene derivative by hydrothermal route to detect biologically pertinent Zn2+ ions. Surface modification of CDs enhances fluorescence efficiency apart from introducing active surface sites broadening its sensor capabilities. The obtained surface-functionalized CDs exhibits a strong blue fluorescence under UV light (365 nm) with a quantum yield (Φ) of 56% which is appreciably good. Zn2+ ions get apprehended in the cavity formed due to passivation by Calix[4]arene moeity on the exterior of CDs having profuse -NH2 groups. Addition of Zn2+ ions into the solution of CDs results in remarkable enhancement in the fluorescence intensity attributed to Photo-induced Electron Transfer (PET) "OFF" phenomenon. The CDs based nanosensor exhibited a wide linear response with a detection limit of 7.34 nM. Significantly, CDs were shown to display insignificant cytotoxicity, decent biocompatibility, and virtuous resistance to photo-bleaching, good stability over a wide range of pH, insignificant variation in the emission intensity in the presence of high concentration of salt and excellent bio-labeling ability when tested on E. coli cell lines. Additionally, the detection results of Zn2+ ions obtained in real samples were in complete agreement with that obtained by Atomic Absorption Spectroscopy (AAS), signifying the prospective application of the proposed probe as a selective and sensitive sensor for Zn2+ ions. The proposed sensor was also applied for fluorescence imaging of intracellular Zn2+ ions. 

Retracted: No

PubPeer comments:
 Update: Iu2019m now thinking I misunderstood. Please disregard. ,
Blockade of MUC1 expression by glycerol guaiacolate inhibits proliferation of human breast cancer cells
Authors: J S Smith
C H Baker
S D Konduri
R Madero-Visbal
J Colon
B Isley
Journal: Anti-cancer agents in medicinal chemistry (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: glycerol guaiacolate; breast cancer cell growth; MCF-7; ZR-75-1; therapeutic efficacy
Affiliations: M. D. Anderson Cancer Center Orlando, 6900 Lake Nona Blvd., Orlando, FL 32827, USA.

Abstract:  We sought to determine whether administration of glycerol guaiacolate at an optimal biological dose inhibits human breast cancer cell growth. Human breast cancer MCF-7 and ZR-75-1 cells were treated with glycerol guaiacolate and the therapeutic efficacy and biological activity of this drug was investigated on breast cancer cell growth. MCF-7 cells were injected into the mammary fat pad of overectamized female athymic nude mice. Ten days later, animals were treated with daily intraperitoneal injections of glycerol guaiacolate for six weeks. Tumor size and volume was monitored and immunohistochemistry analysis on MUC1, p21 and ki-67 was performed. Glycerol guaiacolate decreased breast cancer cell growth in a dose-dependent manner, decreased cell migration, and caused G1 cell cycle arrest. Our results demonstrate that glycerol guaiacolate inhibits MUC1 protein and mRNA expression levels and significantly increased p21 expression in human breast cancer cells as well as induced PARP cleavage. Similarly, glycerol guaiacolate inhibited breast tumor growth in vivo as well as enhanced p21 expression and decreased breast tumor cell proliferation (ki-67 expression). Collectively, our results demonstrate that glycerol guaiacolate decreased MUC1 expression and enhanced cell growth inhibition by inducing p21 expression in breast cancer cells. These findings suggest that glycerol guaiacolate may provide a novel and effective approach for the treatment of human breast cancer. 

Retracted: No

PubPeer comments:
 Figure 5: Blue rectangles highlight an area that appears to be visible in two panels in the MUC1 row. ![file] , 
 It is worth pointing out that two panels in this 2010 figure look very similar to panels in a 2018 paper by some of these authors, i.e. George C. Bobustuc et al., Oncotarget 2018, doi: 10.18632 oncotarget.25696 - https: pubpeer.com publications 224D88DC5ED363E77E9270E4A846DA#2 ![file] ,
siRNA targeting of Trop2 suppresses the proliferation and invasion of lung adenocarcinoma H460 cells
Authors: Ai-Gui Jiang
Li-Xin Zhang
Ye-Han Zhu
Xiao-Yan Gao
Hui-Yu Lu
Journal: Experimental and Therapeutic Medicine (2015)
Discipline: CLINICAL MEDICINE
Keywords: Trop2; lung adenocarcinoma; small interfering RNA.

Abstract:  The aim of the present study was to investigate the effect of the small interfering RNA (siRNA)-induced inhibition of the Trop2 gene on the proliferation and invasion of lung adenocarcinoma H460 cells. A recombinant adenovirus expression vector, which contained siRNA targeting open reading frames for Trop2 (rAd5-siTrop2), was transfected into lung adenocarcinoma H460 cells. Three groups were included in the study, namely the Ctrl (non-transfected control), rAd5-siCtrl (native control) and rAd5-siTrop2 (knockdown Trop2 gene) groups. The mRNA and protein expression levels of Trop2 were detected using quantitative polymerase chain reaction and western blot analysis, respectively. In addition, the expression levels of cyclin Dl and phospho-extracellular signal regulated kinase (p-ERK)-1 were detected using western blot analysis. The effects of Trop2 inhibition on the proliferation and invasion of lung adenocarcinoma H460 cells were investigated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assay. Trop2-targeted siRNA recombinant plasmids were successfully constructed. The recombinant adenovirus vector, rAd5-siTrop2, significantly downregulated the mRNA and protein expression levels of Trop2 in the lung adenocarcinoma H460 cells, with cyclin D1 and p-ERK-1 expression downregulated simultaneously. In addition, following the silencing of Trop2, the proliferation and invasion rates of the lung adenocarcinoma H460 cells were reduced. Therefore, the results indicated that Trop2 serves a key function in the proliferation and invasion of lung adenocarcinoma H460 cells in vitro. 

Retracted: No

PubPeer comments:
 This paper was found during a systematic search of papers in this journal with possible duplicated images. About 10% of the papers in this journal (n=169 examined) were found to contain inappropriately duplicated images. These papers have all been reported to the journal publisher in 2017. The editors promised to  investigate promptly but no action has been taken as of today. Figure 5. * Red boxes: Panels A (Ctrl) and B (rAd50Ctrl-siRNA) appear to show an overlap if one of the panels is mirrored. ![file] ,
<p>SOX17 Inhibits Tumor Metastasis Via Wnt Signaling In Endometrial Cancer</p>
Authors: Guiqiang Du
Yongli Zhang
Weiqiang Zhou
Junjie Qu
Jingyun Wang
Kai Wang
Journal: OncoTargets and Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: SOX17; endometrial cancer (EC); high-mobility group (HMG); migration.
Affiliations: Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China.

Abstract:  Background: Endometrial cancer (EC) is the most common gynecological malignancy with high incidence of metastasis, while the mechanism of metastasis in EC is not clear. Methods: Immunohistochemistry and real-time PCR assays were used to assess expression of SOX17 in paraffin-embedded tissues from EC patients and in EC cells. The migration of EC cells was assessed by wound-healing and Transwell assays as well as in an in vitro study of nude mice. In addition, the expression of specific proteins was analyzed by Western blot. Results: We observed that SOX17 expression levels were relatively high in stage I EC specimens, and were significantly correlated with the epithelial cadherin (E-cadherin) and β-catenin expression. Additionally, stage II EC patients whose specimens had relatively high SOX17 expression levels had better outcomes. Wound-healing and Transwell assays and in vivo murine experiments revealed that SOX17 inhibited EC cell migration. Meanwhile, SOX17 increased expression of E-cadherin and decreased expression of β-catenin and proteins in the Wnt signaling pathway. Moreover, LiCl (β-catenin activator) enhanced the regulatory effects of SOX17 on the expression of E-cadherin, promigratory cadherin, vimentin, and proteins in the Wnt signaling pathway, while XAV93920 (β-catenin inhibitor) exerted the opposite effect. The SOX17 N-terminus was proved to be necessary for these effects. Mechanistic investigations suggested SOX17 inhibits EC cell migration by inactivating the Wnt/β-catenin-epithelial mesenchymal transition (EMT) axis in EC cells. Conclusion: We uncovered a common SOX17-β-catenin-EMT mechanism underlying EC cell migration. 

Retracted: No

PubPeer comments:
 Figure 3 has issues. See 3A, 3B and 3G. Box locations are approximate. *** ![file] *** ![file] ,
A long-acting β2-adrenergic agonist increases the expression of muscarine cholinergic subtype‑3 receptors by activating the β2-adrenoceptor cyclic adenosine monophosphate signaling pathway in airway smooth muscle cells
Authors: Ni-Wen Huang
Gang Wang
Song-Ze Wu
Yuan-Hua Liu
Chun-Tao Liu
Journal: Molecular Medicine Reports (2015)
Discipline: CLINICAL MEDICINE
Keywords: β2‑adrenergic agonists; severe asthma; bronchoprotection tolerance; formoterol; muscarinic M3 receptor
Affiliations: Department of Respiratory and Critical Care Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China., Pneumology Group, Department of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.

Abstract:  The persistent administration of β2‑adrenergic (β2AR) agonists has been demonstrated to increase the risk of severe asthma, partly due to the induction of tolerance to bronchoprotection via undefined mechanisms. The present study investigated the potential effect of the long‑acting β2‑adrenergic agonist, formoterol, on the expression of muscarinic M3 receptor (M3R) in rat airway smooth muscle cells (ASMCs). Primary rat ASMCs were isolated and characterized following immunostaining with anti‑α‑smooth muscle actin antibodies. The protein expression levels of M3R and phospholipase C‑β1 (PLCβ1) were characterized by western blot analysis and the production of inositol 1,4,5‑trisphosphate (IP3) was determined using an enzyme‑linked immunosorbent assay. Formoterol increased the protein expression of M3R in rat ASMCs in a time‑ and dose‑dependent manner, which was significantly inhibited by the β2AR antagonist, ICI118,551 and the cyclic adenosine monophosphate (cAMP) inhibitor, SQ22,536. The increased protein expression of M3R was positively correlated with increased production of PLCβ1 and IP3. Furthermore, treatment with the glucocorticoid, budesonide, and the PLC inhibitor, U73,122, significantly suppressed the formoterol‑induced upregulated protein expression levels of M3R and PLCβ1 and production of IP3. The present study demonstrated that formoterol mediated the upregulation of M3R in the rat ASMCs by activating the β2AR‑cAMP signaling pathway, resulting in increased expression levels of PLCβ1 and IP3, which are key to inducing bronchoprotection tolerance. Administration of glucocorticoids or a PLC antagonist prevented formoterol‑induced bronchoprotection tolerance by suppressing the protein expression of M3R. 

Retracted: No

PubPeer comments:
 Figure 7A and 7B appear to show the same actin band for different treatments. *** ![file] *** Enhanced brightness ![file] , 
 See retraction of paper with similar authors: https: pubpeer.com publications CF1009244393768F196C54297F4751 ,
lncRNA-XLOC_012370 Promotes the Development of Pancreatic Cancer and Inactivates the NF-κB Pathway Through miR-140-5p
Authors: Xiao-Qian Wang
Han-Xiao Nie
Li Wang
Bai-Shun Wan
Feng Han
Tao He
Ling Zhang
Journal: Frontiers in Oncology (2021)
Discipline: CLINICAL MEDICINE
Keywords: NF-κB signal pathway; TLR4; lncRNA-XLOC_012370; miR-140-5p; pancreatic cancer.
Affiliations: Department of Hepatopancreatobiliary Surgery, Henan Tumor Hospital Affiliated to Zhengzhou University, Zhengzhou, China.

Abstract:  Pancreatic cancer is a high incidence, high degree of malignancy, and high mortality in the digestive system tumor. The incidence of pancreatic cancer in China has increased nearly six folds in the past 20 years, ranking fifth in the mortality rate of malignant tumors, so it is particularly important to actively explore clinical indicators with better diagnostic significance for pancreatic cancer. LncRNA performs an essential regulatory function in the occurrence, development, and metastasis of many kinds of tumors, playing both a carcinogenic role and a tumor suppressor gene. Here, we demonstrated the function and mechanism of LncRNA-XLOC_012370 in the development of pancreatic cancer. In our research, the abnormal upregulation of XLOC_012370 was observed in pancreatic cancer patients' tumor tissues. XLOC_012370 was related to tumor stage, lymph node metastasis, and overall survival. Silencing of XLOC_012370 prevented the proliferation, migration, and invasion via the NF-κB signal pathway. Further, miR-140-5p was identified as the target and downstream of XLOC_012370 and involved in pancreatic cancer progression. In vivo, knockdown of XLOC_012370 inhibited tumor growth via the NF-κB signal pathway. In conclusion, lncRNA-XLOC_012370 is closely related to some malignant clinicopathological features and prognosis of pancreatic cancer. Thus the miR-140-5p/NF-κB signal pathway might represent a promising treatment strategy to combat pancreatic cancer. 

Retracted: Yes

PubPeer comments:
 Retracted [29 December 2021] . H t [RetractionWatch] . ---------------------------------- The journal and Chief Editors retract the 23 February 2021 article cited above. Following publication, concerns were raised regarding the validity of the data in the article. The authors failed to provide the raw data or a satisfactory explanation during the investigation, which was conducted in accordance with Frontiersu2019 policies. Given the concerns, and the lack of raw data, the editors no longer have confidence in the findings presented in the article. u200b This retraction was approved by the Chief Editors of Frontiers in Oncology and the Chief Executive Editor of Frontiers. The authors have not responded to any correspondence regarding the retraction. ----------------------------- It would be helpful to learn more about the  concerns that were raised , and who raised them. ,
PNPLA3 overexpression results in reduction of proteins predisposing to fibrosis
Authors: Giorgio Rossi
Cristina Russo
Saverio Massimo Lepore
Luca Valenti
Stefano Romeo
Benedetta Maria Motta
Arturo Pujia
Piero Pingitore
Olov Wiklund
Paola Dongiovanni
Andrea Caddeo
Marica Meroni
Tiziana Montalcini
Rosellina Margherita Mancina
Serena Pelusi
Journal: Human molecular genetics (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Liver fibrosis; hepatic stellate cells; PNPLA3; TGF-β; lipid droplets
Affiliations: Department of Molecular and Clinical Medicine, University of Gothenburg, Sweden., Internal Medicine, Fondazione IRCCS Ca' Granda Ospedale Policlinico Milano, Milan, Italy., Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy., Clinical Nutrition Unit, Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy., Liver Surgery and Transplant Unit, Fondazione IRCCS Ca' Granda Ospedale Policlinico Milano, Milan, Italy., Cardiology Department, Sahlgrenska University Hospital, Gothenburg, Sweden.

Abstract:  Liver fibrosis is a pathological scarring response to chronic hepatocellular injury and hepatic stellate cells (HSCs) are key players in this process. PNPLA3 I148M is a common variant robustly associated with liver fibrosis but the mechanisms underlying this association are unknown. We aimed to examine a) the effect of fibrogenic and proliferative stimuli on PNPLA3 levels in HSCs and b) the role of wild type and mutant PNPLA3 overexpression on markers of HSC activation and fibrosis.Here, we show that PNPLA3 is upregulated by the fibrogenic cytokine transforming growth factor-beta (TGF-β), but not by platelet-derived growth factor (PDGF), and is involved in the TGF-β-induced reduction in lipid droplets in primary human HSCs. Furthermore, we show that retinol release from human HSCs ex vivo is lower in cells with the loss-of-function PNPLA3 148M compared with 148I wild type protein. Stable overexpression of PNPLA3 148I wild type, but not 148M mutant, in human HSCs (LX-2 cells) induces a reduction in the secretion of matrix metallopeptidase 2 (MMP2), tissue inhibitor of metalloproteinase 1 and 2 (TIMP1 and TIMP2), which is mediated by retinoid metabolism. In conclusion, we show a role for PNPLA3 in HSC activation in response to fibrogenic stimuli. Moreover, we provide evidence to indicate that PNPLA3-mediated retinol release may protect against liver fibrosis by inducing a specific signature of proteins involved in extracellular matrix remodelling. 

Retracted: No

PubPeer comments:
 *[left]* Fig 5 from [Xu et al (2020)] .  Effect of miRNA-196b inhibitor transfection on HepD2 cell apoptosis . *[right]* Fig 2F from [Sun et al (2018)] .  The efficiencies of cell apoptosis in Bel-7402 and HepG2 cells after miR-5692a knockdown . ![file] Could the authors comment on the similarities among the marked panels? ,
Study of miR-143 expression in stomach cancer
Authors: Zeng Liu
Wen-Rong Fu
Shao-Jun Huang
Qing-Feng Li
Yu-Fang Zhu
Zhao-Yuan Li
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: apoptosis; miR-143; proliferation; stomach cancer.
Affiliations: Department of Medical Laboratory, Xiangyang Central Hospital, The Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441021, P.R. China., Department of Oncology, Xiangyang Central Hospital, The Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441021, P.R. China., Department of Pathology, Xiangyang Central Hospital, The Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441021, P.R. China.

Abstract:  The present study was planned to investigate miR-143 expression during stomach cancer. The study explored the relationship between miR-143 expression and clinicopathological characteristics including proliferation, migration and apoptosis of stomach cancer cells. Sixty-three samples from each of stomach cancer tissue and surrounding tissue were obtained. Total RNA was extracted. The expression levels of miR-143 from stomach cancer tissue as well as from surrounding tissue were measured by semi-quantitative PCR. The effects of miR-143 overexpression on the migration of stomach cancer cells were examined by Transwell assay. The effects of miR-143 overexpression on the apoptosis of stomach cancer cells were examined by flow cytometer. The expression level of miR-143 was significantly decreased in stomach cancer tissues in comparison to surrounding tissues (P&lt;0.01). Moreover, the expression of miR-143 related well with the tumor size, TNM stage, lymphatic metastasis and relapse (P&lt;0.01). On the other hand, stomach cancer cell line with overexpression of miR-143, showed significant decline in proliferation rate and migration rate comparison to control cells (P&lt;0.01). However, it showed significant higher in apoptosis rate (P&lt;0.01). The present study concluded that expression of miR-143 is low during stomach cancer. Further, higher expression levels of miR-143 have the ability to decline proliferation and migration of stomach cancer cells. In this manner, the expression level of miR-143 could be used as an important factor to determine the severity of stomach cancer. 

Retracted: No

PubPeer comments:
 Some unexpected repeated features in the flow cytometry plot in Figure 6a. The email address for the last author bears no resemblance to their name. *** ![file] , 
 Fig 1A, 3A.  The expression levels of miR-143 in stomach cancer tissue and surrounding tissue. (A) Agarose gel electrophoresis ...  Agarose gel electrophoresis showed the expression of overexpressed miR-143 in MGC-803 cells . ![file] GAPDH loading controls appear to be the same in these unrelated experiments. ,
Exosomes derived from Fusobacterium nucleatum-infected colorectal cancer cells facilitate tumour metastasis by selectively carrying miR-1246/92b-3p/27a-3p and CXCL16
Authors: Ge Zhang
Fangfang Chen
Wan-Li Liu
Jun Chen
Songhe Guo
Qiuyao Zeng
Journal: Gut (2020)
Discipline: CLINICAL MEDICINE
Keywords: colorectal cancer.
Affiliations: Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China., Department of Clinical Laboratory Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China., State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China., Department of Clinical Laboratory Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China  ., Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China  .

Abstract:  Objective: Exosomes released from tumour cells are packed with unique RNA and protein cargo, and they are emerging as an important mediator in the communication network that promotes tumour progression. The facultative intracellular bacterium Fusobacterium nucleatum (Fn) is an important colorectal cancer (CRC)-associated bacterium. To date, the function of exosomes from Fn-infected CRC cells has not been explored. Design: Exosomes were isolated by sequential differential centrifugation and verified by transmission electron microscopy, NanoSight analysis and Western blotting. Given that exosomes have been shown to transport miRNAs and proteins to alter cellular functions, we performed miRNA sequencing and proteome analysis of exosomes from Fn-infected and non-infected cells. The biological role and mechanism of exosomes from Fn-infected cells in CRC tumour growth and liver metastasis were determined in vitro and in vivo. Results: We demonstrated that exosomes delivered miR-1246/92b-3p/27a-3p and CXCL16/RhoA/IL-8 from Fn-infected cells into non-infected cells to increase cell migration ability in vitro and promote tumour metastasis in vivo. Finally, both circulating exosomal miR-1246/92b-3p/27a-3p and CXCL16 levels were closely associated with Fn abundance and tumour stage in patients with CRC. Conclusion: This study suggests that Fn infection may stimulate tumour cells to generate miR-1246/92b-3p/27a-3p-rich and CXCL16/RhoA/IL-8 exosomes that are delivered to uninfected cells to promote prometastatic behaviours. 

Retracted: No

PubPeer comments:
 The results of this article are based on the article published in Science  RNA-Mediated Metal-Metal Bond Formation in the Synthesis of Hexagonal Palladium Nanoparticles in 2004. This article was retracted and it was later proved that RNA did not catalyze the formation of Palladium Hexagons and the particles were infact just precursor particles. The big question arise how results of this article correct when the result of base paper in science has been proved incorrect. The authors must answer this very important question or the journal must retract this also. ,
Long non-coding RNA FOXD3-AS1 silencing exerts tumor suppressive effects in nasopharyngeal carcinoma by downregulating FOXD3 expression via microRNA-185-3p upregulation
Authors: Jiang Hu
Jun Pan
Dan Wang
Qiwen Duan
Zhiguo Luo
Journal: Cancer Gene Therapy (2021)
Discipline: CLINICAL MEDICINE
Keywords: Nasopharyngeal carcinoma; lncRNA FOXD3-AS1; miR-185-3p; FOXD3; malignancies
Affiliations: Department of Oncology, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, P.R. China. ., Department of Pediatrics, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, P.R. China., Department of Oncology, Taihe Hospital, Hubei University of Medicine, 442000, Shiyan, P.R. China.

Abstract:  Emerging evidence indicates that the incidence of nasopharyngeal carcinoma (NPC) remains high in endemic regions despite changing environmental factors, suggesting that genetic traits contribute to its development. Recently, long non-coding RNA-microRNA-messenger RNA (lncRNA-miRNA-mRNA) axis has been reported to be implicated in the pathophysiological processes of malignancies. Moreover, initial bioinformatic analysis revealed a highly expressed lncRNA Forkhead box D3 antisense RNA1 (FOXD3-AS1) for mechanistic network underlying NPC in this present study. Therefore, this study aims to delineate the ability of lncRNA FOXD3-AS1 to influence the NPC progression. The relationship among lncRNA FOXD3-AS1, miR-185-3p, and FOXD3 was identified with bioinformatics prediction, dual-luciferase reporter gene assays, RNA-binding protein immunoprecipitation, and RNA pull-down assays. Furthermore, effects of lncRNA FOXD3-AS1 on malignant phenotypes in vitro, alongside tumor formation in vivo, of transfected NPC stem-like cells were examined with gain- and loss-of-function experiments. Our findings revealed that lncRNA FOXD3-AS1 and FOXD3 exhibited increased expression levels, while miR-185-3p exhibited diminished levels in NPC. The levels of lncRNA FOXD3-AS1 and FOXD3 were further correlated with tumor node metastasis stage and pathological type of patients with NPC. LncRNA FOXD3-AS1 was also confirmed to negatively regulate the miR-185-3p expression, which further targeted the downstream gene FOXD3. In addition, lncRNA FOXD3-AS1 knockdown repressed cell stemness, colony formation, viability, invasion, migration, and in vivo tumor growth, and accelerated cell apoptosis. Moreover, FOXD3 silencing or miR-185-3p overexpression reversed the effects of lncRNA FOXD3-AS1. Our findings provide evidence indicating that lncRNA FOXD3-AS1 could bind to miR-185-3p to upregulate the FOXD3 expression, thereby promoting the development of NPC. 

Retracted: No

PubPeer comments:
 Of the three gene sequences (forward) I checked in Table 1, two of them were incorrect (NCBI nucleotide blast with filter for Homo Sapiens). Furthermore, it is interesting to note that all Western immunoblotting data are presented as bar graphs. No raw data are presented, even not as supplementary data. The anonymous e-mail address to the corresponding authors with not association to neither the scientist nor institution. ![file] ,
Identification of miR-1293 potential target gene: TIMP-1
Authors: Tengfei Chen
Yunyun Ma
Guojun Zhang
Heying Chu
Guoqiang Zhao
Ping Li
Huaqi Wang
Yuanyuan Wang
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TIMP-1; miR-1293; regulation; biological processes; cell growth
Affiliations: Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, No.1, Jianshe Road, Zhengzhou, 450052, China.

Abstract:  Tissue inhibitor of metalloproteinases 1 (TIMP-1) is a glycosylated protein with multiple activities in the regulation of biological processes, such as cell growth and apoptosis as well as tumor invasion and metastasis. Bioinformatics analysis using TargetScan and miRanda suggested tissue inhibitors of TIMP-1 are among the targets of miR-1293. To confirm this, we cloned both wild-type and mutant TIMP-1 3'UTR fragments by overlap extension PCR, constructed the recombinant plasmids pGL3-TIMP-1-wt, -mut, and pcDNA 3.1(+)/TIMP-1-CDS and, respectively, co-transfected them into 293T cells with the miR-1293 inhibitor, mimics or the miR inhibitor-NC using a BTX ECM 2001 square-wave electroporator. We used a luciferase assay to investigate binding of miR-1293 to the 3'UTR of TIMP-1. Effects on the levels of the TIMP-1 protein were analyzed by Western blot experiments. The luciferase reporter assay showed a statistically significant (P &lt; 0.05) upregulation of activity. Western blot analysis showed a significant increase of expression of the TIMP-1 gene co-transfected with the miR-1293 inhibitor, and demonstrated direct binding of miR-1293 to the 3'UTR of TIMP-1. In this study, we identified TIMP-1 as a novel direct target for miR-1293, which provides the basis for further study of the multifunctional mechanisms of miR-1293 and TIMP-1 in the regulation of a variety of diseases. 

Retracted: No

PubPeer comments:
  Fig. 1 Overlap extension PCR amplification of the TIMP-1-wt and -mut genes and restriction analysis of recombinant plasmids by electrophoresis and sequencing . 1(a) and 1(b) seem to use the same molecular-ladder reference lane, though flipped horizontally. Doesn t this defeat the purpose of including a reference lane within each gel? ![file] , 
 Fig 2(c).  Western blot analysis of TIMP1 expression in transfected cells. b-Actin was used as an endogenous reference . ![file] Below: Fig 4(b) from [Wang et al (2014)] , with largely overlapping authorship.  Western blot analysis of PDCD4 expression in transfected cells. GAPDH was used as the endogenous reference . The marked lanes are surprisingly similar, apart from the greater detail in the former. Is it possible, despite the lapse of time, for authors to upload the original scans? , 
 [Perhaps a systemic problem] . Journals and readers may wish to proceed with caution. ,
Effects of miR-155 on hypertensive rats via regulating vascular mesangial hyperplasia
Authors: Z Cheng
R Liao
X-X Wang
D Xu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Vascular smooth muscle cell; proliferation; hypertension; p27; miR-155
Affiliations: Department of Cardiology, The First Branch, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. .

Abstract:  Objective: Vascular smooth muscle cell (VSMC) excessive proliferation is related to hypertension. The cell cycle inhibitory factor (p27) can arrest cell cycle, while its down-regulation is associated with hypertension. It is found that microRNA-155 (miR-155) plays a regulatory role in VSMC proliferation, while its relationship with hypertension is still unclear. Bioinformatics analysis reveals the targeted relationship between miR-155 and the 3'-UTR of p27 mRNA. This study aims to explore the role of miR-155 in regulating p27 expression, VSMC proliferation and apoptosis, and the pathogenesis of hypertension. Materials and methods: Dual luciferase reporter gene assay confirmed the relationship between miR-155 and p27. MiR-155, p27, α-smooth muscle actin (α-SMA), and Ki-67 expressions in the thoracic aorta media of rat hypertension model were detected. VSMCs were cultured in vitro and divided into five groups, including anti-miR-NC, anti-miR-155, pIRES2-blank, pIRES2-p27, and anti-miR-155 + pIRES2-p27 groups. Cell cycle was evaluated by using flow cytometry. Cell proliferation was detected with EdU staining. Hypertension rats were randomly divided into antagomir-155 and antagomir-control. Caudal artery systolic and diastolic pressures were measured. Results: MiR-155 targeted suppressed p27 expression. MiR-155 and Ki-67 expressions significantly enhanced, while p27 and α-SMA levels reduced in the tunica media from hypertension rats compared with control. Down-regulation of miR-155 and/or up-regulation of p27significantly declined cell proliferation and arrested cell cycle in G1 phase. Antagomir-155 injection markedly decreased systolic and diastolic pressures, elevated p27 and α-SMA expressions in media, and reduced the thickness of tunica media. Conclusions: MiR-155 promoted VSMC proliferation by targeting p27. MiR-155 enhancement was related to hypertension. MiR-155 played a therapeutic effect on hypertension. 

Retracted: No

PubPeer comments:
 This paper has features suggestive of [what has elsewhere been labeled as  Papermill #2 ] , characterised by stylised geometrical WBs that are reduced to sharp-edged black ovals on a featureless grey background, reminiscent of a Miro painting: ![file] ![file] Other examples are listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit?usp=sharing One curious feature of this papermill is the frequent mismatch between the name of the putative corresponding author and the email address provided for correspondence. ![file] ,
Binding of DCC by netrin-1 to mediate axon guidance independent of adenosine A2B receptor activation
Authors: E Stein
M Tessier-Lavigne
Y Zou
M Poo
Journal: Science (2001)
Discipline: Multidisciplinary
Keywords: Netrins; Axon growth; DCC proteins; Receptors; Signaling
Affiliations: Department of Anatomy, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143-0452, USA.

Abstract:  Netrins stimulate and orient axon growth through a mechanism requiring receptors of the DCC family. It has been unclear, however, whether DCC proteins are involved directly in signaling or are mere accessory proteins in a receptor complex. Further, although netrins bind cells expressing DCC, direct binding to DCC has not been demonstrated. Here we show that netrin-1 binds DCC and that the DCC cytoplasmic domain fused to a heterologous receptor ectodomain can mediate guidance through a mechanism involving derepression of cytoplasmic domain multimerization. Activation of the adenosine A2B receptor, proposed to contribute to netrin effects on axons, is not required for rat commissural axon outgrowth or Xenopus spinal axon attraction to netrin-1. Thus, DCC plays a central role in netrin signaling of axon growth and guidance independent of A2B receptor activation. 

Retracted: No

PubPeer comments:
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 It has been five years, and there still has not been any action by the journal. The paper keeps on being cited, so it is still relevant and it would be great if these concerns could be looked into. I agree with the concerns raised above, and will recap them here and add my own findings. Figure 3A (contrast enhanced) * Bands are surrounded by sharp transitions that might not be compression artifacts (see comment #1) * Yellow boxes: A background area in the top left panel appears to be visible two times within the same photo (see comments #1 and #4) * Green boxes: A background area in the bottom left panel appears to be visible two times within the same photo (a new finding). ![file] These findings are supported by Forensically (default settings): ![file] , 
 Figure 3C. * Bands are surrounded by sharp transitions that might not be compression artifacts (see comment #1) * Red boxes: the bottom left panel appears to show the same background area twice (see comment #3) * Blue boxes: the top right panel appears to show the same background area twice, but 180 degrees rotated (a new finding) ![file] The red-boxed findings are supported by Forensically (which cannot detect rotated duplications): ![file] Both blue- and red-boxed findings are picked up by ImageTwin: ![file] , 
 Returning to this paper, which still seems to be unaddressed, there may also be a gel slice used in 2 different figures in Figure 3, more easily identified after a change in the aspect ratio. *** ![file] *** Close-up ![file] ,