PReD-Bench/PRed-Bench huggingface dataset:
Construction of p66Shc gene interfering lentivirus vectors and its affections on alveolar epithelial cells apoptosis induced by hyperoxia
Authors: Chan Zhang
Xiao-Ping Lei
Wen-Bin Dong
Lan Kang
Xue-Song Zhai
Shuai Zhao
Qing-Ping Li
Lin Guo
Journal: Drug Design Development and Therapy (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: RNA interference; alveolar epithelial cells; apoptosis; hyperoxia; lentiviral vector
Affiliations: Department of Newborn Medicine, Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, People's Republic of China.

Abstract:  Background: The aim of this study is to observe the inhibitive effects of p66Shc gene interfering lentivirus vectors on the expression of p66Shc, and to explore its effects on alveolar epithelial cells apoptosis induced by hyperoxia. Methods: The gene sequences were cloned into the pLenR-GPH-shRNA lentiviral vector, which was selected by Genebank searches. The pLenR-GPH-shRNA and lentiviral vector packaging plasmid mix were cotransfected into 293T cells to package lentiviral particles. Culture virus supernatant was harvested, and then the virus titer was determined by serial dilution assay. A549 cells were transduced with the constructed lentiviral vectors, and real-time polymerase chain reaction (RT-PCR) and Western blot were used to evaluate p66Shc expression. This study is divided into a control group, a hyperoxia group, an A549-p66ShcshRNA hyperoxia group, and a negative lentivirus group. Cell apoptosis was detected by flow cytometry after 24 hours; the expression of X-linked inhibitor of apoptosis protein (XIAP) and caspase-9 were detected by immunohistochemistry assay. The production of reactive oxygen species and cellular mitochondria membrane potential (ŒîŒ®m) were determined by fluorescence microscopy. Results: We successfully established the p66Shc gene interfering lentivirus vectors, A549-p66ShcshRNA. The A549-p66ShcshRNA was transfected into alveolar epithelial cells, and the inhibitive effects on the expression of p66Shc were observed. Both RT-PCR and Western blot demonstrated downregulation of p66Shc expression in A549 cells. In the A549-p66ShcshRNA hyperoxia group, we found dampened oxidative stress. A549-p66ShcshRNA can cause p66Shc gene silencing, reduce mitochondrial reactive oxygen species generation, reduce membrane potential decrease, reduce the apoptosis of A549 cells, and reduce alveolar epithelial cell injury, while the lentiviral empty vector group had no such changes. Conclusion: p66Shc gene interfering lentivirus vector can affect the alveolar epithelial cells apoptosis induced by hyperoxia. 

Retracted: No

PubPeer comments:
 Figure 1c includes sharp edges potentially indicative of splicing, which is not explicitly mentioned in the caption. Could the authors provide an uncropped original? ***  *** Inverted image  *** Full figure  , 
 Correction 1 15 2020 line added to indicate splicing.  ,
Regulatable adenovector harboring the GFP and Yamanaka genes for implementing regenerative medicine in the brain
Authors: Gustavo R Morel
Martina Canatelli-Mallat
Priscila Chiavellini
Marianne Lehmann
Paula C Reggiani
Rodolfo G Goya
Claudia B Here√±√∫
Journal: Gene Therapy (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Biological rejuvenation; partial cell reprogramming; regulatable pluripotency gene expression systems; adenovector; humanized green fluorescent protein (GFP)
Affiliations: Institute for Biochemical Research (INIBIOLP)-Histology B & Pathology B, School of Medicine, National University of La Plata, La Plata, Argentina., Institute for Experimental Pharmacology Cordoba (IFEC), School of Chemical Sciences, National University of Cordoba, Cordoba, Argentina., Institute for Biochemical Research (INIBIOLP)-Histology B & Pathology B, School of Medicine, National University of La Plata, La Plata, Argentina. .

Abstract:  Biological rejuvenation by partial cell reprogramming is an emerging avenue of research. In this context, regulatable pluripotency gene expression systems are the most widely used at present. We have constructed a regulatable bidirectional adenovector expressing the humanized green fluorescent protein (GFP) and oct4, sox2, klf4, and c-myc genes (known as the Yamanaka genes or OSKM). The OSKM genes are arranged as a bicistronic tandem (hSTEMCCA tandem), which is under the control of a Tet-Off bidirectional promoter that also controls the expression of the gFP gene. Separately, a constitutive cassette expresses the regulatory protein tTA. Vector DNA was transfected in HEK293 Cre cells, which were additionally infected with the helper adenovector H14, unable to package its DNA due to the Cre recombinase produced by the HEK293 Cre cells. The newly generated vector was expanded by six iterated coinfections of the above cells which were lysed at the end of the process and the adenovector purified by ultracentrifugation in a CsCl gradient. The titer of the initial preparation was 1.2 √ó 1012 physical viral particles/ml. As expected, GFP fluorescence in vector-transduced rat fibroblast cultures declined with the dose of doxycycline (DOX) present in the medium. Immunocytochemical analysis of transduced cells confirmed the expression of the four Yamanaka genes. Additionally, 3 days after vector injection in the hypothalamus of rats, a significant level of fluorescence was observed in the region. Addition of 2 mg/ml DOX to the drinking water reduced the GFP expression. This adenovector constitutes a promising tool for implementing nonintegrative partial cell reprogramming. 

Retracted: No

PubPeer comments:
 Figure 3: Panels showing untreated cells appear to be surprisingly similar after contrast is increased (see below). Would the authors please comment?  ,
Alpha-synuclein lowers p53-dependent apoptotic response of neuronal cells. Abolishment by 6-hydroxydopamine and implication for Parkinson's disease
Authors: Erwan Paitel
Cristine Alves Da Costa
Bruno Vincent
Fr√©d√©ric Checler
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: alpha-synuclein; TSM1 neuronal cells; apoptotic stimulus; caspase 3; DNA fragmentation
Affiliations: Institut de Pharmacologie Mol√©culaire et Cellulaire du CNRS, UMR6097, 660 route des Lucioles, 06560 Valbonne, France.

Abstract:  We have examined the influence of alpha-synuclein on the responsiveness of TSM1 neuronal cells to apoptotic stimulus. We show that alpha-synuclein drastically lowers basal and staurosporine-stimulated caspase 3 immunoreactivity and activity. This is accompanied by lower DNA fragmentation and reduced number of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)-positive neurons. Interestingly, alpha-synuclein also diminishes both p53 expression and transcriptional activity. We demonstrate that the antiapoptotic phenotype displayed by alpha-synuclein can be fully reversed by the Parkinson's disease-associated dopamine derivative 6-hydroxydopamine. Thus, 6-hydroxydopamine fully abolishes the alpha-synuclein-mediated reduction of caspase 3 activity and reverses the associated decrease of p53 expression. 6-Hydroxydopamine triggers thioflavin T-positive deposits in alpha-synuclein, but not mock-transfected TSM1 neurons, and drastically increases alpha-synuclein immunoreactivity. Altogether, we suggest that alpha-synuclein lowers the p53-dependent caspase 3 activation of TSM1 in response to apoptotic stimuli and we propose that the natural toxin 6-hydroxydopamine abolishes this antiapoptotic phenotype by triggering alpha-synuclein aggregation, thereby likely contributing to Parkinson's disease neuropathology. 

Retracted: No

PubPeer comments:
null, 
null, 
 How to explain same tubulin bands in figures 1 (figure 2 was mislabelled, it should be figure 1) and 6, yet different treatments? https: imgur.com vqXhIBc , 
 There are three groups of similar bands in Fig. 1 and Fig. 6, shown in red, blue and green boxes respectively.  ,
Long noncoding RNA SOX2OT contributes to gastric cancer progression by sponging miR-194-5p from AKT2
Authors: Fei Qu
Peilong Cao
Journal: Experimental Cell Research (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: AKT2; Gastric cancer; LncRNA SOX2OT; miR-194-5p.
Affiliations: Department of Pathology, Jinan Central Hospital affiliated to Shandong University, 105 Jiefang Road, Jinan 250013, Shandong province, China. Electronic address: ., Department of Pathology, the First Affiliated Hospital of Xi'an Jiaotong University School, Xi'an 710061, China.

Abstract:  Gastric cancer (GC) is a highly malignant cancer with poor prognosis. Long non-coding RNA (LncRNA) may play an important role in tumor progression. Our present study aimed to explore the effect of LncRNA SOX2OT on GC progression. We observed that SOX2OT was overexpressed in GC tissues and cell lines. Overexpressed SOX2OT promoted cell proliferation and metastasis of GC cells (SGC-7901, TMK-1) and the phosphorylation of AKT2 as well, while knockdown of SOX2OT reversed these effects. Besides that, miR-194-5p was predicted to be a target of SOX2OT and decreased expression of miR-194-5p was observed in GC tissues and cell lines. Overexpressed miR-194-5p counteracted the promoting role of SOX2OT on cell proliferation and invasion of GC cells. Moreover, AKT2 was predicted to be a target of miR-194-5p. The expression of AKT2 was negatively regulated by miR-194-5p while positively regulated by SOX2OT. Overexpressed AKT2 also promoted GC cell proliferation and invasion. Our in vitro experiments suggested that SOX2OT promoted cell proliferation and metastasis of GC cells via sponging miR-194-5p from AKT2. Finally, our in vivo experiments indicated that overexpressed SOX2OT promoted GC tumor growth and metastasis in nude mice. Taken together, our present study suggested that SOX2OT contributed to GC progression via sponging miR-194-5p from AKT2 both in vitro and in vivo. The SOX2OT-miR-194-5p-AKT2 axis may provide a new perspective for treatment of GC. 

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 black blobs on a featureless grey background, reminiscent of a Miro painting:  ...and by a small repertoire of recurring flow cytometry plots,  slightly modified by artisanal stippling on each of their occurrences.  Other examples are listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit?usp=sharing The connection between the name of the nominal corresponding author and the corresponding email address is not obvious.  ,
Development and evaluation of tripalmitin emulsomes for the treatment of experimental visceral leishmaniasis
Authors: Suresh P Vyas
Ajay Pal
Swati Gupta
Anuradha Dube
Anil Jaiswal
Journal: Journal of liposome research (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Amphotericin B; Emulsomes; Macrophage targeting; Visceral leishmaniasis; O-palmitoyl mannan
Affiliations: Nanomedicine Research Center, Department Of Pharmaceutics, I.S.F. College Of Pharmacy , Moga 142 001 (PB) , INDIA.

Abstract:  The antifungal and antileishmanial agent amphotericin B (AmB) was formulated in tripalmitin based nanosize lipid partices (emulsomes) for macrophage targeting for the treatment of visceral leishmaniasis (VL). Emulsomes were modified by coating them with macrophage-specific ligand (O-palmitoyl mannan, OPM). The antileishmanial activity of AmB (0.5 and 1 mg/kg) was investigated in-vivo against VL by the inhibition of parasitic load in the spleen of L. donovani infected hamsters after intraperitoneal injections of AmB-Doc (Mycol), plain emulsomes (TPEs) and OPM coated emulsomes (TPEs-OPM). The formulations were found to be less effective at the dose of 0.5 mg/kg. At the dose of 1 mg/kg, formulation TPEs-OPM eliminated intracellular amastigotes of L. donovani within splenic macrophages more efficiently (62.76 ¬± 3.54 % parasite inhibition) than the formulation TPEs (42.68 ¬± 2.36 % parasite inhibition) (P &lt; 0.01) or AmB-Doc (25.87 ¬± 3.87 % parasite inhibition) (P &lt; 0.001). Our results suggest that these formulations (plain and ligand grafted emulsomes) are a promising substitute to the conventional AmB-Doc formulation for the treatment of VL. 

Retracted: Yes

PubPeer comments:
 Figure 5. Much more similar than you would expect. https: imgur.com KnwtH8S ,
Retracted : Curcumin ameliorates atherosclerosis through upregulation of miR‚Ä?26
Authors: Dajun Sun
Yezhou Li
Leilei Tian
Dexin Yin
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: VEGF; arteriosclerosis; curcumin; miR-126.
Affiliations: Department of Vascular Surgery China‚ÄêJapan Union Hospital of Jilin University Changchun China, Operating Room China‚ÄêJapan Union Hospital of Jilin University Changchun China

Abstract:  The potential usage of curcumin in diverse human diseases has been widely studied, including arteriosclerosis (AS). This study focused on investigating the relationship between curcumin and AS-associated microRNA, which may provide a better understanding of curcumin in a different mechanism. Human microvascular endothelial HMEC-1 cells were treated by curcumin alone or oxidized low-density lipoprotein (ox-LDL) plus curcumin, after which the following parameters were analyzed: cell viability, migration, and the expression of AS-associated factors. The regulatory effects of curcumin on miR-126 and signaling pathways involved in AS were then studied. Further, an animal model of AS was stimulated by feeding rabbits with 1% cholesterol diet. The effects of curcumin on the animal model were explored. We found that curcumin treatment significantly reduced HMEC-1 cells viability, migration, and the protein levels of MMP-2, MMP-9, and vascular endothelial growth factor (VEGF) in the presence or absence of ox-LDL. Meanwhile, the expression of VEGFR1 and VEGFR2 was repressed by curcumin. miR-126 was upregulated by curcumin. The abovementioned effects of curcumin on HMEC-1 cells were all attenuated when miR-126 was silenced. And also, VEGF was a target gene of miR-126, and curcumin could inhibit the activation of PI3K/AKT JAK2/STAT5 signaling pathways via miR-126. The effects of curcumin and its regulation on miR-126 and VEGF were confirmed in the animal model of AS. To sum up, curcumin exerted potent anti-AS property possibly via upregulating miR-126 and thereby inhibiting PI3K/AKT and JAK2/STAT5 signaling pathways. 

Retracted: Yes

PubPeer comments:
 Tables 2 (particles prepared in water) and 3 (prepared in PBS) appear to share a lot of numbers in certain positions of the numbers, such as the first or the third digit. I have marked those with boxes of the same color. Can the authors please share the original measurements?  , 
 Means in Table 3 minus Means in Table 2 are odd...  , 
 Dear Elisabeth, More than appreciated for pointing out these issues. We terribly apologize for such errors and will seriously check all of the raw data related to this article and respond as soon as possible. Sincerely Bingyang ,
Activation of PTGS2 /NF‚ÄêŒ∫B signaling pathway enhances radiation resistance of glioma
Authors: Guifang Zhao
Yimeng Dai
Libo Wang
Liang Liu
Weiyao Wang
Xiaoyang Liu
Ling Qi
Cheng Tan
Journal: Cancer Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: PTGS2; NF-Œ∫B signaling pathway; glioma; radiation resistance.
Affiliations: Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China., Department of Pathophysiology, Jilin Medical University, Jilin, China.

Abstract:  Objective: We focused on the effects of PTGS2/NF-Œ∫B signaling pathway on the radiation resistance of glioma in the study. Methods: We downloaded the microarray data from the Gene Expression Omnibus (GEO) database. We verified transfection successfully through QRT-PCR analysis. Immunofluorescence was used to detect Œ≥H2AX content under 2 Gy radiation. The survival rates of cells under 2 Gy irradiation were tested by clonogenic survival assay. Flow cytometry was used to detect cell cycle. Western blot was applied to detect the expression of NF-Œ∫B pathway-related proteins. We also used MTT assay to detect the proliferation of cells. Results: In this research, we discovered that the expression of the PTGS2 was upregulated in radiation-resistant glioma cells. The radio-tolerance rate of U87 cells was obviously elevated after the overexpression of PTGS2. The radioresistance of U87R cells was significantly reduced after the knockdown of PTGS2. After radiotherapy, the number of cells arrested in G2/M phase decreased after PTGS2 overexpression in U87cells but increased in PTGS2 knockdown in U87R cells. The survival rate of U87 and U87R cells under radiation decreased significantly after the addition of NF-Œ∫B inhibitor. The proliferation of U87 cells was suppressed by radiation and the addition of Bay 11. In addition, PTGS2 activated NF-Œ∫B signaling pathway and prevented DNA damage after radiotherapy. Lastly, PTGS2 was proved to facilitate tumor cell proliferation and improve the radio-tolerance. Conclusion: PTGS2/NF-Œ∫B signaling pathway was involved in radio-tolerance of glioma cells, which provided a new insight into glioma therapy. 

Retracted: No

PubPeer comments:
  [Clistoabdominalis Helluo commented] And now, blots recycled from a different paper:   The parallel paper with Figs 5B, 5D is [Heldsinger et al (2012)] . ,
DNA damage signals through differentially modified E2F1 molecules to induce apoptosis
Authors: Laurie A Seifried
Jasmyne Carnevale
Oliva Palander
Frederick A Dick
Journal: Molecular and Cellular Biology (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: E2F transcription; cell proliferation; apoptosis; DNA double-strand breaks; cell cycle arrest
Affiliations: London Regional Cancer Program, London, Ontario, Canada.

Abstract:  E2F transcription can lead to cell proliferation or apoptosis, indicating that E2Fs control opposing functions. In a similar manner, DNA double-strand breaks can signal to induce cell cycle arrest or apoptosis. Specifically, pRB is activated following DNA damage, allowing it to bind to E2Fs and block transcription at cell cycle promoters; however, E2F1 is simultaneously activated, leading to transcription at proapoptotic promoters. We examined this paradoxical control of E2F transcription by studying how E2F1's interaction with pRB is regulated following DNA damage. Our work reveals that DNA damage signals create multiple forms of E2F1 that contain mutually exclusive posttranslational modifications. Specifically, E2F1 phospho-serine 364 is found only in complex with pRB, while E2F1 phosphorylation at serine 31 and acetylation function to create a pRB-free form of E2F1. Both pRB-bound and pRB-free modifications on E2F1 are essential for the activation of TA-p73 and the maximal induction of apoptosis. Chromatin immunoprecipitation demonstrated that E2F1 phosphorylated on serine 364 is also present at proapoptotic gene promoters during the induction of apoptosis. This indicates that distinct populations of E2F1 are organized in response to DNA damage signaling. Surprisingly, these complexes act in parallel to activate transcription of proapoptotic genes. Our data suggest that DNA damage signals alter pRB and E2F1 to engage them in functions leading to apoptotic induction that are distinct from pRB-E2F regulation in cell cycle control. 

Retracted: No

PubPeer comments:
 Figure 5E. Much more similar than expected.  ,
Lentiviral gene therapy vectors encoding VIP suppressed diabetes-related inflammation and augmented pancreatic beta-cell proliferation
Authors: Salih Sanlioglu
Fulya Erendor
Elif Ozgecan Sahin
Mustafa Kemal Balci
Thomas S Griffith
Ahter D Sanlioglu
Journal: Gene Therapy (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Type 1 diabetes; autoimmune condition; insulin-producing beta cells; pancreas; hyperglycemia
Affiliations: Department of Gene and Cell Therapy, Akdeniz University, Faculty of Medicine, 07058, Antalya, Turkey., Department of Internal Medicine, Division of Endocrinology and Metabolism, Akdeniz University Faculty of Medicine, 07058, Antalya, Turkey., Department of Urology, University of Minnesota, School of Medicine, Minneapolis, MN, 55455, USA., Department of Gene and Cell Therapy, Akdeniz University, Faculty of Medicine, 07058, Antalya, Turkey. .

Abstract:  Type 1 diabetes (T1DM) is an autoimmune condition in which the immune system attacks and destroys insulin-producing beta cells in the pancreas leading to hyperglycemia. Vasoactive intestinal peptide (VIP) manifests insulinotropic and anti-inflammatory properties, which are useful for the treatment of diabetes. Because of its limited half-life due to DPP-4-mediated degradation, constant infusions or multiple injections are needed to observe any therapeutic benefit. Since gene therapy has the potential to treat genetic diseases, an HIV-based lentiviral vector carrying VIP gene (LentiVIP) was generated to provide a stable VIP gene expression in vivo. The therapeutic efficacy of LentiVIP was tested in a multiple low-dose STZ-induced animal model of T1DM. LentiVIP delivery into diabetic animals reduced hyperglycemia, improved glucose tolerance, and prevented weight loss. Also, a decrease in serum CRP levels, and serum oxidant capacity, but an increase in antioxidant capacity were observed in LentiVIP-treated animals. Restoration of islet cell mass was correlated with an increase in pancreatic beta-cell proliferation. These beneficial results suggest the therapeutic effect of LentiVIP is due to the repression of diabetes-induced inflammation, its insulinotropic properties, and VIP-induced beta-cell proliferation. 

Retracted: No

PubPeer comments:
 Figure 6: Magenta boxes show an overlap. Both of these are labelled as control, but I guess they re not supposed to show sections of the same image? Would the authors please check?  ,
p62 is a key regulator of nutrient sensing in the mTORC1 pathway
Authors: Juan F Linares
Maria T Diaz-Meco
Angeles Duran
Shadi Abu-Baker
Malene Hansen
Jayashree Joshi
Aleksey Porollo
Jorge Moscat
Ramars Amanchy
Journal: Molecular Cell (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p62; raptor; mTORC1 complex; amino acid signaling; S6K1
Affiliations: Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92307, USA.

Abstract:  The signaling adaptor p62 is a critical mediator of important cellular functions, owing to its ability to establish interactions with various signaling intermediaries. Here, we identify raptor as an interacting partner of p62. Thus, p62 is an integral part of the mTORC1 complex and is necessary to mediate amino acid signaling for the activation of S6K1 and 4EBP1. p62 interacts in an amino acid-dependent manner with mTOR and raptor. In addition, p62 binds the Rags proteins and favors formation of the active Rag heterodimer that is further stabilized by raptor. Interestingly, p62 colocalizes with Rags at the lysosomal compartment and is required for the interaction of mTOR with Rag GTPases in vivo and for translocation of the mTORC1 complex to the lysosome, a crucial step for mTOR activation. 

Retracted: No

PubPeer comments:
 Figure 4C: More similar than expected, could authors check please?  Zoom(contrast enhanced):  , 
 Dear Colleague, Thanks for your message. We will check the raw data and come back soon with a response. , 
 Dear Colleague, We have reviewed the original films of the raw data of this experiment. Please find attached new scans of the original films of the notebooks of the lab (year 2010) demonstrating that each blot correspond to negative results of p18, p14 and MP1 in endogenous immunoprecipitation of p62 . We have also included the corresponding scans of the cell lysates. Thanks so much for your interest in our work. Best regards, Jorge  , 
 #3 It s absolutely obvious those three panels highlighted by *Stachys Mucronata* in #1 are the same and have been duplicated. Thus a correction of the paper would be mandatory. Film scans posted by Dr. Moscat in #3 are at low resolution, therefore are irrelevant in clarifying the issue. ,
Long non-coding RNA ROR1-AS1 enhances colorectal cancer metastasis by targeting miR-375
Authors: F-Z Wang
M-Q Zhang
L Zhang
M-C Zhang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNAs; tumorigenesis; colorectal cancer; ROR1-AS1; RT-qPCR
Affiliations: Department of Emergency, Tianjin Union Medical Center, Tianjin, China. .

Abstract:  Objective: Recent research has proved that long non-coding RNAs (lncRNAs) play an important role in tumorigenesis. In this research, lncRNA ROR1-AS1 was explored to identify its role in the development of colorectal cancer (CRC). Patients and methods: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to measure ROR1-AS1 expression of CRC tissues. Besides, function assays including wound healing assay and transwell assay were conducted to detect the effect of ROR1-AS1 on the metastasis of CRC. Furthermore, Luciferase assays and RNA immunoprecipitation assay (RIP) were used to explore the underlying mechanism. Results: By comparison with ROR1-AS1 expression in adjacent tissues, the ROR1-AS1 expression level was significantly higher in CRC samples. Moreover, loss of ROR1-AS1 inhibited cell migration and cell invasion of CRC cells. Besides, gain of ROR1-AS1 enhanced cell migration and cell invasion of CRC cells. Furthermore, it was found that ROR1-AS1 acted as a competing endogenous RNA via sponging miR-375 in CRC. Conclusions: The present study suggests that ROR1-AS1 could promote cell migration and invasion of CRC by sponging miR-375, which may offer a potential therapeutic target in CRC. 

Retracted: Yes

PubPeer comments:
 Figure 3, several bands appear to be replicated (see same colors) and used to represent different samples and treatments. There are also sharp lines (arrows). Original image contrast was adjusted to see band patterns more clearly. https: imgur.com a 7ETXs5A , 
 Could the author clarify the apparent band duplication? https: imgur.com a 7ETXs5A ,
Retracted : Knockdown of long non‚Äêcoding RNA MEG3 protects H9c2 cells from hypoxia‚Äêinduced injury by targeting microRNA‚Ä?83
Authors: Yaliang Tong
Hong Chang
Haiming Xu
Licheng Gong
Gongliang Guo
Tao Zhang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MEG3; acute myocardial infarction; hypoxia; microRNA-183; p27.
Affiliations: Department of Cardiovascular Internal Medicine, China-Japan Union Hospital of Jilin University, Changchun, China., Department of Gastrointestinal Surgery, China-Japan Union Hospital of Jilin University, Changchun, China.

Abstract:  Acute myocardial infarction (AMI) occurs when blood supply to the heart is diminished (ischemia) for long time, and ischemia is primarily caused due to hypoxia. This study evaluated the effects of long non-coding RNA maternally expressed gene 3 (MEG3) on hypoxic rat cardiomyocyte-drived H9c2 cells. Hypoxic injury was confirmed by alterations of cell viability, migration, invasion, apoptosis, and hypoxia-inducible factor 1Œ± (HIF-1Œ±) expression. MEG3 level in hypoxic cells and effects of its knockdown on hypoxic cells were assessed. The interactions between MEG3 and miR-183 as well as miR-183 and p27 were investigated. In addition, the effects of aberrantly expressed MEG3, miR-183, and p27 on hypoxic cells along with the activation of PI3K/AKT/FOXO3a signaling pathway were all assessed. Results showed that hypoxia induced decreases of cell viability, migration and invasion, and increases of apoptosis and expressions of HIF-1Œ± and MEG3. Knockdown of MEG3 decreased hypoxia-induced injury in H9c2 cells. Knockdown of MEG3 also increased miR-183 expression, which was identified as a target of MEG3. The effects of MEG3 knockdown on the hypoxic cells were reversed by miR-183 silence. p27 was identified as a target gene of miR-183, and its expression negatively regulated by miR-183. The mechanistic studies revealed that knockdown of p27 decreased hypoxia-induced H9c2 cell injury by activating PI3K/AKT/FOXO3a signal pathways. These findings suggest that knockdown of MEG3 alleviates hypoxia-induced H9c2 cell injury by miR-183-mediated suppression of p27 through activation of PI3K/AKT/FOXO3a signaling pathway. 

Retracted: Yes

PubPeer comments:
 The label of Z axis does not match the title of Fig. 17(b). Could the authors address this issue?  ,
Synthesis and biological evaluation of modified laminin peptide (N2S2-KDP) with enhanced affinity for neuronal growth and targeted molecular imaging (SPECT)
Authors: Anil K Mishra
Raunak Varshney
Meenakshi Saklani
Ankur Kaul
Anjani K Tiwari
Sweta Singh
Aruna Kaushik
Roger Stromberg
Puja P Hazari
Rashi Mathur
Journal: Bioorganic Chemistry (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Dosimetry; KDP; Molecular modeling; Neutrite growth; Peptide
Affiliations: Division of Cyclotron and Radiopharmaceutical Sciences, Institute of Nuclear Medicine and Allied Sciences, Delhi 110054, India. Electronic address: ., Division of Cyclotron and Radiopharmaceutical Sciences, Institute of Nuclear Medicine and Allied Sciences, Delhi 110054, India., Department of Biosciences and Nutrition at Novum, Karolinska Institute, S-14183 Huddinge, Sweden.

Abstract:  An analog of Œ≥1 laminin (RDIAEIIKDI) decapeptide has been used to augment neuronal survival and regeneration after injuries, during aging and other CNS disorder. As a prime synthetic peptide, KDI, is responsible for the neurite outgrowth of human embryonic neurons. In this study, we have designed, modified a KDI derivative and synthesized by replacing isoleucine (I) with Pro (P) amino acid at C-terminal to enhance its potency towards neurite growth. -Cys-Gly-Cys (-CGC) N2S2 motif was also incorporated in the present design for peptide radiolabeling. The modified peptide showed a better binding with the desired 3T1M receptor for neurite growth. The peptide was synthesized using solid phase peptide synthesis and Fmoc-strategy with more than 80% yield. The receptor binding studies of 99mTc-N2S2-KDP in Neuro2A cell lines showed Kd value in 31 nM range and the complex showed appreciable brain uptake in mice. The results on human SH-SY5Y indicate that the unlabeled N2S2-KDP may perhaps be useful for neurite growth in neurodegenerative disorder. 

Retracted: No

PubPeer comments:
 Sibling blot for Bcl2 and p21. One can see rotation of blot.  ,
CBX7 and miR-9 are part of an autoregulatory loop controlling p16(INK) (4a)
Authors: Gordon Peters
Sharon Brookes
Nadine Martin
Ana O&#x27;Loghlen
Jes√∫s Gil
Valentina Rapisarda
Journal: Aging Cell (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CBX7; Polycomb; miR-9; p16INK4a; senescence.
Affiliations: Cell Proliferation Group, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Campus, London, W12 0NN, UK., Molecular Oncology Laboratory, CRUK London Research Institute, 44 Lincoln's Inn Fields, London, WC2A 3LY, UK., Epigenetics & Cellular Senescence Group, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, 4 Newark Street, London, E1 2AT, UK.

Abstract:  Polycomb repressive complexes (PRC1 and PRC2) are epigenetic regulators that act in coordination to influence multiple cellular processes including pluripotency, differentiation, cancer and senescence. The role of PRCs in senescence can be mostly explained by their ability to repress the INK4/ARF locus. CBX7 is one of five mammalian orthologues of Drosophila Polycomb that forms part of PRC1. Despite the relevance of CBX7 for regulating senescence and pluripotency, we have a limited understanding of how the expression of CBX7 is regulated. Here we report that the miR-9 family of microRNAs (miRNAS) downregulates the expression of CBX7. In turn, CBX7 represses miR-9-1 and miR-9-2 as part of a regulatory negative feedback loop. The miR-9/CBX7 feedback loop is a regulatory module contributing to induction of the cyclin-dependent kinase inhibitor (CDKI) p16(INK4a) during senescence. The ability of the miR-9 family to regulate senescence could have implications for understanding the role of miR-9 in cancer and aging. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
 2017 erratum. https: onlinelibrary.wiley.com doi full 10.1111 acel.12554 In the article u2018CBX7 and miRu20109 are part of an autoregulatory loop controlling p16INK4au2019, the two lower panels of Figure 6C are duplicated. The correct Figure 6 with the new shp16 control image in panel C is shown below. The authors would like to apologize for any inconvenience caused. ,
Silencing of a novel lncRNA LOC105369748 suppresses the progression of hepatocellular carcinoma by sponging miR‚Ä?095 from MBD2
Authors: Changyong E
Hang Li
Jinghui Yang
Chunsheng Li
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HCC; LOC105369748; MBD2; lncRNA; miR-5095.
Affiliations: Department of Hepatobiliary and Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun, China., Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun, China., Department of Cerebral Surgery, Jilin Cancer Hospital, Changchun, China.

Abstract:  A growing number of studies have suggested that long noncoding RNAs (lncRNAs) play critical roles in human malignant cancers, including hepatocellular carcinoma (HCC). However, the functions of most lncRNAs have not been elucidated in HCC. In the present study, we explored the potential functions of a novel lncRNA LOC105369748 in the HCC progression. We identified that LOC105369748 expression was significantly elevated in HCC tissues compared with normal tissues based on bioinformatics analysis, quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis and in situ hybridization (ISH) examination. Moreover, we found that the LOC105369748 overexpression was associated with poor prognosis in patients with HCC. Then we measured the effects of LOC105369748 on HCC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT). And our results demonstrated that LOC105369748 exerted oncogenic roles. In terms of mechanism, LOC105369748 was shown to promote MBD2 expression through competitively binding to microRNA(miR)-5095 in HCC. In conclusion, our findings elucidate that the LOC105369748/miR-5095/MBD2 signaling axis regulates the HCC progression and may be a novel therapeutic avenue. 

Retracted: No

PubPeer comments:
 1.tThis paper doesnu2019t have a section for statistics 2.tNot a single word u201cstatisticsu201d or u201cstatisticalu201d used anywhere in the whole manuscript 3.tHow the SD values in table and the error bars in the figures were purposed? 4.tWhat does error bar indicate in Figure-3 ? SD, SEM or something else ? 5.tNo statistics or error bar in Fig. 2. a. for the cytotoxicity (MTT) assay ? 6.tFig. 4. B control show an uncanny similarity with Figure 4.a of previous publication (Varshney, et al.: Def. Life SCI. J., Vol. 1, No. 1, June 2016, DOI : 10.14429 dlsj.1.10062) without mentioning any citation, reference or permission.  ,
lncRNA RMRP Prevents Mitochondrial Dysfunction and Cardiomyocyte Apoptosis via the miR-1-5p/hsp70 Axis in LPS-Induced Sepsis Mice
Authors: Hongyan Xie
Xiaoquan Lai
Shiqing Wei
Yixin Cai
Zhenling Wang
Ying Han
Min Xu
Kun Tan
Journal: Inflammation (2020)
Discipline: IMMUNOLOGY
Keywords: HSPA4; cardiomyocyte; lncRNA RMRP; miR-1-5p; sepsis.
Affiliations: Department of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China., Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. .

Abstract:  Both long non-coding RNA (lncRNA) RMRP and heat shock protein (HSP) 70 have been known to play crucial roles in inflammation. The present study investigated the roles of lncRNA RMRP and HSP70 protein 4 (HSPA4) in lipopolysaccharide (LPS)-induced sepsis. The C57BL/6 mice were treated with LPS, following which the cardiomyocytes were isolated for in vitro experiments. Further, a cardiac muscle cell line, HL-1 was transfected with plasmids expressing RMRP and HSPA4, si-NC, si-HSPA4, miR-1-5p mimic, and controls in vitro. Cell apoptosis, mitochondrial membrane potential (MMP), and levels of intracellular reactive oxygen species (ROS), mRNAs, and proteins were detected in the transfected mice tissues and cells. The LPS treatment significantly reduced the expression levels of RMRP, MMP, and mitochondrial cytochrome C. Moreover, it enhanced the cardiomyocyte apoptosis, intracellular ROS levels, cytoplasm cytochrome C levels, and the expression of caspase-3 and caspase-9 and nuclear factor Œ∫B (NF-Œ∫B) p65 subunit. The predicted RMRP-miR-1-5p-HSPA4 network was validated by co-transfection experiments in vitro in HL-1 cells. The transfection of miR-1-5p-treated cells with pcDNA-RMRP enhanced the levels of the protein HSPA4; however, no change at the mRNA level was observed. Moreover, miR-1-5p mimic attenuated the protective effect of pcDNA-HSPA4 against LPS-induced mitochondrial damage and apoptosis. In addition, we observed that silencing of HSPA4 increased the expression of nuclear p65; however, this effect could be reversed by co-transfection with pcDNA-RMRP. The lncRNA RMRP axis acts as a sponge for miR-1-5p. RMRP inhibits LPS-induced apoptosis of cardiomyocytes and mitochondrial damage by suppressing the post-transcriptional regulatory function of miR-1-5p on HSPA4. We believe that RMRP exhibits therapeutic potential for LPS-induced myocardial dysfunction both in vitro and in vivo. 

Retracted: No

PubPeer comments:
 In Figure 2E, 3C and 6B, Western immunoblotting data have been duplicated and presented as something else.  ,
Lack of detectable neoantigen depletion signals in the untreated cancer genome
Authors: Erik Larsson
Alejandro Jim√©nez-S√°nchez
Martin L Miller
Jimmy Van den Eynden
Journal: Nature genetics (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Somatic mutations; neoantigens; HLA molecules; negative selection pressure; neoantigen depletion
Affiliations: Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. ., Department of Human Structure and Repair, Anatomy and Embryology Unit, Ghent University, Ghent, Belgium. ., Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge, UK. ., Cancer Research UK Cambridge Institute, University of Cambridge, Li Ka Shing Centre, Robinson Way, Cambridge, UK., Program for Computational and Systems Biology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA., Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Abstract:  Somatic mutations can result in the formation of neoantigens, immunogenic peptides that are presented on the tumor cell surface by HLA molecules. These mutations are expected to be under negative selection pressure, but the extent of the resulting neoantigen depletion remains unclear. On the basis of HLA affinity predictions, we annotated the human genome for its translatability to HLA binding peptides and screened for reduced single nucleotide substitution rates in large genomic data sets from untreated cancers. Apparent neoantigen depletion signals become negligible when taking into consideration trinucleotide-based mutational signatures, owing to lack of power or to efficient immune evasion mechanisms that are active early during tumor evolution. 

Retracted: No

PubPeer comments:
 Figure 1A: All three FACS plots are identical  , 
 **CORRECTION** https: www.frontiersin.org articles 10.3389 fimmu.2021.778085 full ,
Synthesis of benzylidenemalononitrile by Knoevenagel condensation through monodisperse carbon nanotube-based NiCu nanohybrids
Authors: Hakan Burhan
Nursefa Zengin
Haydar G√∂ksu
Fatih ≈ûen
Aysun ≈ûavk
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Nickel/copper nanohybrids; Multi-walled carbon nanotubes; Knoevenagel condensation; Ultrasonic hydroxide assisted reduction method; X-ray diffraction
Affiliations: Kaynasli Vocational College, Duzce University, D√ºzce, 81900, Turkey., Sen Research Group, Biochemistry Department, Faculty of Arts and Science, Dumlupƒ±nar University, Evliya √áelebi Campus, 43100, K√ºtahya, Turkey., Kaynasli Vocational College, Duzce University, D√ºzce, 81900, Turkey. ., Sen Research Group, Biochemistry Department, Faculty of Arts and Science, Dumlupƒ±nar University, Evliya √áelebi Campus, 43100, K√ºtahya, Turkey. .

Abstract:  Monodisperse nickel/copper nanohybrids (NiCu@MWCNT) based on multi-walled carbon nanotubes (MWCNT) were prepared for the Knoevenagel condensation of aryl and aliphatic aldehydes. The synthesis of these nanohybrids was carried out by the ultrasonic hydroxide assisted reduction method. NiCu@MWCNT nanohybrids were characterized by analytical techniques such as X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), transmission electron microscopy (TEM), high-resolution transmission electron microscopy (HR-TEM), and Raman spectroscopy. According to characterization results, NiCu@MWCNT showed that these nanohybrids form highly uniform, crystalline, monodisperse, colloidally stable NiCu@MWCNT nanohybrids were successfully synthesized. Thereafter, a model reaction was carried out to obtain benzylidenemalononitrile derivatives using NiCu@MWCNT as a catalyst, and showed high catalytic performance under mild conditions over 10-180 min. 

Retracted: No

PubPeer comments:
 This paper is one of 40+ (42 and counting) papers by the same research group that all share the same photo. In all papers, this photo is used as a zoomed-in inset representing the high-resolution transmission electron microscopy (HRTEM) analysis of the  atomic lattice fringe and particle size of the nanoparticles. Of concern, the same photo is used to represent a different type of nanoparticle in each of these papers. Here is a collage of 6 different uses of the same photo,  Inset 1 :  A list of the first 30 papers that all use this photo, and the different types of nanoparticles that they represent can e.g. be found here: * Betuu0308l Su0327en et al. - DOI: 10.1016 j.ijhydene.2018.03.175 - https: pubpeer.com publications 8AD71F4A32472314CCE9983D47E36F Of note, this is a different set of papers than the 15 papers by the same group that all appear to use another HRTEM image called  Inset 2 . For an example of that photo and the list of the first 14 papers identified in that set, see DOI: 10.1016 j.ijhydene.2017.05.113 https: pubpeer.com publications CAD2F16435F6C639F5DE6851A2E61D Here is Figure 2 of this paper, which includes the  Inset 1 photo:  ,
MicroRNA-183-5p suppresses the malignant progression of osteosarcoma via binding to AKT
Authors: S Yuan
Q-R Qian
J Zhu
J-H Shao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-183-5p; osteosarcoma; AKT; proliferation; migration
Affiliations: Department of Joint Surgery and Orthopedic Medicine, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China. .

Abstract:  Objective: To clarify the role of microRNA-183-5p in the malignant progression of osteosarcoma (OS) and the potential mechanism. Patients and methods: Relative level of microRNA-183-5p in 40 paired OS tissues and matched normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between microRNA-183-5p level and clinical indexes of OS patients was analyzed. By transfection of microRNA-183-5p mimics in SaOS-2 and MG63 cells, changes in proliferation and migration were evaluated. The potential target of microRNA-183-5p was verified by dual-luciferase reporter gene assay. Finally, the biological function of protein kinase B (AKT) in OS progression mediated by microRNA-183-5p was detected. Results: MicroRNA-183-5p was downregulated in OS tissues compared to controls. Relative to OS patients with high expression of microRNA-183-5p, those with low expression had a higher rate of distant metastasis and lower overall survival. Transfection of microRNA-183-5p mimics attenuated proliferative and migratory abilities of SaOS-2 and MG63 cells. AKT was upregulated in OS and negatively correlated to microRNA-183-5p. Overexpression of AKT could abolish the inhibitory effect of microRNA-183-5p on proliferative and migratory abilities of OS cells. Conclusions: MicroRNA-183-5p is closely related to distant metastasis and poor prognosis of OS. It suppresses the malignant progression of OS by targeting AKT. 

Retracted: No

PubPeer comments:
 Figure 2C. * Green boxes: Two panels appear to overlap.  , 
 Figure 2D. * Yellow boxes: Two panels appear to overlap, with a surprising 90 degree rotation.  , 
  A total of 40 OS patients were enrolled in this study, including 24 males and 16 females (6-48 years, mean age of 26.24u00b16.58 years). Meanwhile, 40 cases of normal bone tissues were surgically resected from hip replacement. No differences in gender and age were observed between OS patients and controls. Wait, what, 40 patients with a mean age of ~26 years required **hip replacements**? What are people doing in Shanghai? , 
 Fig 1D.  Kaplan-Meier curves introduced for survival analysis in OS patients with high expression and low expression of miR-183-5p .  The K-M plots are seemingly constructed of Lego, and show an alarming decline of survival in the lead-up to 75 months. Table 1. The column headings promise to convert the numbers within each half-group into percentages, but do not deliver. The Note makes no sense.  These are among the characteristic features of a papermill, with its products tabulated here: https: docs.google.com spreadsheets d 1_762PbYYTCJhek5PdBuiDuN1q48UDgMa-rT6gi_jA8c edit?usp=sharing ,