PReD-Bench/PRed-Bench huggingface dataset:
Sildenafil increases chemotherapeutic efficacy of doxorubicin in prostate cancer and ameliorates cardiac dysfunction
Authors: Rakesh C Kukreja
Anindita Das
Ian Qureshi
Ray Lee
Clint Mitchell
Paul Dent
Eric Mayton
Fadi N Salloum
David Durrant
Margaret A Park
Nicholas N Hoke
Journal: Proceedings of the National Academy of Sciences of the United States of America (2010)
Discipline: Multidisciplinary
Keywords: sildenafil; phosphodiesterase-5 inhibitor; infarct size reduction; ischemia/reperfusion injury; left ventricular dysfunction
Affiliations: Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University Pauley Heart Center, Richmond, VA 23298, USA. 

Abstract:  We have shown that the potent phosphodiesterase-5 (PDE-5) inhibitor sildenafil (Viagra) induces a powerful effect on reduction of infarct size following ischemia/reperfusion injury and improvement of left ventricular dysfunction in the failing heart after myocardial infarction or doxorubicin (DOX) treatment. In the present study, we further investigated the potential effects of sildenafil on improving antitumor efficacy of DOX in prostate cancer. Cotreatment with sildenafil enhanced DOX-induced apoptosis in PC-3 and DU145 prostate cancer cells, which was mediated by enhanced generation of reactive oxygen species, up-regulation of caspase-3 and caspase-9 activities, reduced expression of Bcl-xL, and phosphorylation of Bad. Overexpression of Bcl-xL or dominant negative caspase 9 attenuated the synergistic effect of sildenafil and DOX on prostate cancer cell killing. Furthermore, treatment with sildenafil and DOX in mice bearing prostate tumor xenografts resulted in significant inhibition of tumor growth. The reduced tumor size was associated with amplified apoptotic cell death and increased expression of activated caspase 3. Doppler echocardiography showed that sildenafil treatment ameliorated DOX-induced left ventricular dysfunction. In conclusion, these results provide provocative evidence that sildenafil is both a powerful sensitizer of DOX-induced killing of prostate cancer while providing concurrent cardioprotective benefit. 

Retracted: No

PubPeer comments:
 The actin is duplicated in Fig 5 D and 5E in two different experimental settings. DU145 cells were infected with Adeno-Bcl-xL in Fig 5D and DU145 cells were infected with Adeno-dnCaspase9 in Fig 5E. The western analyses were done using Bcl-xL and proCaspase9 antibody, respectively. However, the Actin that measured the equal loading was duplicated in both the figures. It should be used separately as they used two different genes for infection or overexpression (technically). ![file] Interestingly, the same actin was used in another paper by the same author in Oncotarget. The experimental setting was completely different. Fig 3 Oncotarget. 2016 Jan 26; 7(4): 4399u20134413. ![file] Can authors explain? ,
<p>LncRNA PTCSC3 Inhibits Tumor Growth and Cancer Cell Stemness in Gastric Cancer by Interacting with lncRNA Linc-pint</p>
Authors: Yu Xu
Junyan Wang
Jing Han
Chengyuan Liu
Yan Liu
Suju Wei
Da Jiang
Minting Ma
Haijuan Wang
Lei Hong
Fan Zhang
Journal: Cancer Management and Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: gastric cancer; growth; lncRNA Linc-pint; lncRNA PTCSC3; stemness.
Affiliations: Department of Medical Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, People's Republic of China., Examination and Training Center Health and Family Planning Commission of Hebei, Shijiazhuang, Hebei 050051, People's Republic of China.

Abstract:  Background: The tumor suppressor role of lncRNA PTCSC3 has been reported in papillary thyroid carcinoma, our study aimed to investigate its involvement in gastric cancer. Methods: Tumor tissues and adjacent healthy tissues were collected from gastric cancer patients. Expression of PTCSC3 and lncRNA Linc-pint in these tissues was analyzed by RT-qPCR. The interaction between PTCSC3 and Linc-pint was analyzed by overexpression experiments. Cell proliferation and stemness were analyzed by CCK-8 assay and cell stemness assay, respectively. Results: PTCSC3 and lncRNA Linc-pint were both downregulated in tumor tissues than in adjacent healthy tissues of gastric cancer patients. Low levels of PTCSC3 and Linc-pint were closely correlated with poor survival. PTCSC3 and Linc-pint overexpression inhibited tumor growth and cancer cell stemness, while Linc-pint knockdown played an opposite role an attenuated the effects of PTCSC3 overexpression. Expression levels of PTCSC3 and Linc-pint were significantly correlated in tumor tissues but not in adjacent healthy tissues. Overexpression of PTCSC3 and Linc-pint upregulated the expression of each other. Conclusion: PTCSC3 inhibits tumor growth and cancer cell stemness in gastric cancer by interacting with lncRNA Linc-pint. 

Retracted: No

PubPeer comments:
  **Low Levels of PTCSC3 and Linc-pint in Cancer Tissue Indicate Poor Survival** Based on the expression levels of PTCSC3 and Linc-pint in tumor tissues, patients were divided into high (n=36) and low (n=42) PTCSC3 level groups, as well as high (n=38) and low (n=40) Linc-pint level groups according to Youdenu2019s index. Survival curves were plotted based on Kaplanu2013Meier method and compared by **log-rank t test.** As shown in Figure 2A, patients in low-level PTCSC3 group showed significantly lower overall survival rate compared with patients in high PTCSC3 group (Figure 2A). In addition, the overall survival rate of patients in low Linc-pint level group was also significantly lower than that of patients in high Linc-pint level group (Figure 2B). The  log rank t test for comparing K-M survival curves is perhaps a garbled form of the  log rank test . ,
Regulation of miRNAs on c-met protein expression in ovarian cancer and its implication
Authors: Q Si
H Liu
S-R Li
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: HGF/c-met signal pathway; miRNAs; gene regulation; bioinformatics; ovarian cancer
Affiliations: Departments of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, The Inner Mongolia Autonomous Region Tumor Hospital, The Inner Mongolia Autonomous Region Hohhot, China. .

Abstract:  Objective: HGF/c-met signal pathway exerts important roles in tumor pathogenesis. The study of c-met related regulatory mechanism provides the basis for finding anti-tumor molecular drugs. MiRNAs can effectively regulate gene expression and work as gene therapy. The identification of miRNAs for c-met regulation and study of related mechanism are of critical importance. Materials and methods: Bioinformatics approach was used to search for possible miRNAs with regulatory functions on c-met gene. Using pcDNA3.1-EGFP as the scaffold, miRNAs over-expression and inhibitor plasmids were constructed for electroporation-transfection in ovarian cell line ES-2, and pcDNA3.1-EGFP empty plasmid was used as the control group. qRT-PCR and Western blot were applied to measure c-met mRNA and protein expression, followed by transwell chamber in vitro assay for the evaluation of invasion potency. Results: Bioinformatics prediction showed favorable regulatory function on c-met gene by miR-204. The differential expressions of EGFP were observed between pcDNA3.1-EGFP-204-up and inhibitor plasmid pcDNA3.1-EGFP-204-down. After transfection for 24 h and 48 h, c-met expression in miR-204 over-expression group gradually decreased (p&lt;0.05 compared to control group), accompanied with reducing cell migration or invasion potency in a time dependent manner (p&lt;0.05). In contrast, no significant difference in the level of c-met was found in the inhibitor group and control group (p&gt;0.05). Conclusions: The up-regulation of miR-204 suppressed the expression of c-met in ovarian cancer cells and inhibited cell infiltration. The suppression of miR-204 expression, however, presented no significant impact on cell infiltration potency. 

Retracted: No

PubPeer comments:
 Figure 5. * Blue boxes: The left and center image appear to show an overlap. ![file] ,
Repeated olanzapine treatment mitigates PTSD like symptoms in rats with changes in cell signaling factors
Authors: Nagannathahalli Ranga Reddy
Sairam Krishnamurthy
Journal: Brain Research Bulletin (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: BDNF; CREB; Caspase -3; ERK; Olanzapine
Affiliations: Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P., 221 005, India., Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, U.P., 221 005, India. Electronic address: .

Abstract:  Post Traumatic Stress Disorder is an anxiety disorder with prolonged distortion of rational behavior. In this study, we report the preclinical potential of olanzapine (OLZ) in the treatment of PTSD. Since the atypical antipsychotics have modulating effects on cell protective and destructive factors, we tested the effects of OLZ in PTSD regarding these cell modulating factors. Rats, when subjected to stress-restress (SRS) model of PTSD, showed a derangement in cell protective factors like the decline in BDNF, ERK, and CREB. While the adversarial factors like caspase-3 were enhanced. Four weeks treatment with OLZ at doses of 1 and 10 mg/kg significantly mitigated the SRS-induced derangement related to PTSD. OLZ at doses of 1 and 10 mg/kg enhanced BDNF, ERK and CREB levels which were reduced by SRS in PTSD animals. Further, at the fore mentioned doses it also inhibited the elevation of caspase-3 a downstream apoptotic factor. Besides, OLZ also showed mitigation in behavioral alterations related to anxiety and memory brought about by PTSD. These effects of OLZ were comparable to that of paroxetine a clinically approved drug for PTSD in terms of biochemical and behavioral assessments indicating its anti-PTSD potential. 

Retracted: No

PubPeer comments:
 Figure 5. Some bands look unexpectedly similar within or between panels. Arrows focus attention on similarities and orientation of those bands. ![file] , 
 Figure 6A. Some bands look unexpectedly similar within or between panels. Arrows focus attention on similarities and orientation of those bands. ![file] , 
 Figures 6 and 7 appear to look remarkably similar as well. ![file] I will leave Figure 8 and 9 for others to look at. , 
 #3 Forensically about had a meltdown after taking a gander Figure 8. *** ![file] , 
 #2 Horizontal symmetry of lanes 2 3 , 5 6 in the ERK 1 2 slice. ![file] ,
miR-217 suppresses proliferation and promotes apoptosis in cardiac myxoma by targeting Interleukin-6
Authors: Jing Zhang
Huimin Xu
Cui Wang
Journal: Biochemical and Biophysical Research Communications (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apoptosis; Cardiac myxoma; IL-6; Proliferation; miR-217.
Affiliations: Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, 475000, China. Electronic address: ., Department of Cardiovascular Medicine, Huaihe Hospital of Henan University, Kaifeng, 475000, China., Department of Geriatric Cardiovascular Medicine, Huaihe Hospital of Henan University, Kaifeng, 475000, China.

Abstract:  Cardiac myxoma (CM) is a prevalent primary cardiac tumor. miR-217 plays a vital role in tumorigenesis of various cancers, however, its role and underlying molecular mechanism in human CM remain poorly understood. Here, we reported that the expression of miR-217 was downregulated in CM tissues and inversely correlated with the expression of Interleukin-6 (IL-6) mRNA. Gain-of-function analysis indicated that overexpression of miR-217 inhibited the proliferation and promoted the apoptosis of the primary CM cells. Bioinformatics analysis showed that IL-6 was a direct target gene of miR-217, which is confirmed by the dual luciferase assays. Moreover, downregulation of IL-6 by small interference RNA (siRNA) mimicked the tumor-suppressive effects of miR-217 in CM. Furthermore, rescue experiments pointed out that restoration of IL-6 expression abrogated the anti-proliferative and pro-apoptotic effect induced by miR-217 overexpression in CM cells. Taken together, we validated that miR-217 could act as a tumor suppressor in CM by directly targeting 3'UTR of IL-6 gene, indicating that manipulation of miR-217 may be a potential therapeutic strategy for CM patients. 

Retracted: No

PubPeer comments:
 Fig 2C.  Flow cytometry assay was performed to investigate the effect of miR-217 on cell apoptosis . ![file] Here is the left-hand panel color-reversed and superimposed upon the right-hand panel. Cyan and red dots are unique to the left-hand and right-hand panels respectively; dots cancel out if they are present in both. ![file] I have concerns. ,
Rad5-dependent DNA repair functions of the Saccharomyces cerevisiae FANCM protein homolog Mph1
Authors: Dana Branzei
Danielle L Daee
Kyungjae Myung
Simonne Longerich
Xiao-feng Zheng
Elisa Ferrari
Patrick Sung
Xiaoyu Xue
Journal: Journal of Biological Chemistry (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Interstrand cross-links; DNA replication; transcription; Fanconi anemia pathway; repair pathway
Affiliations: Genome Instability Section, Genetics, and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA

Abstract:  Interstrand cross-links (ICLs) covalently link complementary DNA strands, block DNA replication, and transcription and must be removed to allow cell survival. Several pathways, including the Fanconi anemia (FA) pathway, can faithfully repair ICLs and maintain genomic integrity; however, the precise mechanisms of most ICL repair processes remain enigmatic. In this study we genetically characterized a conserved yeast ICL repair pathway composed of the yeast homologs (Mph1, Chl1, Mhf1, Mhf2) of four FA proteins (FANCM, FANCJ, MHF1, MHF2). This pathway is epistatic with Rad5-mediated DNA damage bypass and distinct from the ICL repair pathways mediated by Rad18 and Pso2. In addition, consistent with the FANCM role in stabilizing ICL-stalled replication forks, we present evidence that Mph1 prevents ICL-stalled replication forks from collapsing into double-strand breaks. This unique repair function of Mph1 is specific for ICL damage and does not extend to other types of damage. These studies reveal the functional conservation of the FA pathway and validate the yeast model for future studies to further elucidate the mechanism of the FA pathway. 

Retracted: No

PubPeer comments:
 Does anyone understand why in Figure 3D the combined mph1 srs2 double mutant is not sensitized to the 100uM nitrogen mustard as it is clearly shown in Figure 2 (B, C, and D)? ,
Attenuation of frailty in older adults with mesenchymal stem cells
Authors: Luiza Bagno
Victoria Florea
Joshua M Hare
Angela C Rieger
Journal: Mechanisms of Ageing and Development (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: cell-based therapy; frailty; geriatrics; immunosenescence; inflammation
Affiliations: Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL, United States., Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL, United States; Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, United States. Electronic address: .

Abstract:  Aging frailty is a syndrome characterized by a progressive decline in health and clinical symptoms of exhaustion, weight loss, a feeling of slowing down, and a decrease in functional capacity. The biological substrate for frailty is sarcopenia, which is potentiated by chronic inflammation and depletion or impairment of endogenous precursor and stem cells. Current interventions focus on interdisciplinary approaches which include nutritional supplementation, physical exercise, and cognitive intervention. Clinical studies of these preventative approaches have shown inconsistent and modest benefits, further highlighting the unmet clinical need. A variety of pharmacologic and biologic therapies are currently being tested to treat aging. Cell-based therapy represents an attractive option that addresses the pathophysiology of the syndrome. Human allogeneic mesenchymal stem cells (MSCs) which possess immunomodulatory and tissue reparative properties, have been tested in Phase I and Phase II trials. These small early stage studies reveal that allogeneic MSCs administered to frail older adults are feasible to administer, safe and potentially efficacious, ameliorating signs and symptoms of frailty. These studies have formed the basis for larger ongoing trials. Here we review the pathobiology of frailty, and the potential for developing biological strategies to treat this important syndrome. 

Retracted: No

PubPeer comments:
 These bands (under different conditions) were unexpectedly similar. ![file] ,
Epigenome changes in active and inactive Polycomb‐group‐controlled regions
Authors: Achim Breiling
Valerio Orlando
Laura P O&#x27;Neill
Donatella D&#x27;Eliseo
Bryan M Turner
Journal: EMBO reports (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Polycomb group; epigenetic inheritance; transcriptional states; Drosophila; Polycomb repressive complex 1
Affiliations: Dulbecco Telethon Institute, Institute of Genetics and Biophysics CNR Via Pietro Castellino 111 80131 Naples Italy, Chromatin and Gene Expression Group, Institute of Biomedical Research, University of Birmingham Medical School Birmingham B15 2TT UK

Abstract:  The Polycomb group (PcG) of proteins conveys epigenetic inheritance of repressed transcriptional states. In Drosophila, the Polycomb repressive complex 1 (PRC1) maintains the silent state by inhibiting the transcription machinery and chromatin remodelling at core promoters. Using immunoprecipitation of in vivo formaldehyde-fixed chromatin in phenotypically diverse cultured cell lines, we have mapped PRC1 components, the histone methyl transferase (HMT) Enhancer of zeste (E(z)) and histone H3 modifications in active and inactive PcG-controlled regions. We show that PRC1 components are present in both cases, but at different levels. In particular, active target promoters are nearly devoid of E(z) and Polycomb. Moreover, repressed regions are trimethylated at lysines 9 and 27, suggesting that these histone modifications represent a mark for inactive PcG-controlled regions. These PcG-specific repressive marks are maintained by the action of the E(z) HMT, an enzyme that has an important role not only in establishing but also in maintaining PcG repression. 

Retracted: No

PubPeer comments:
 Figure 3c. Much more similar than expected. https: imgur.com bPyhSdf ,
miR-449a inhibits proliferation and invasion by regulating ADAM10 in hepatocellular carcinoma
Authors: Kai Liu
Baoxing Jia
Songyang Liu
Yingchao Wang
Zhe Jin
Wei Zhang
Yahui Liu
Journal: American journal of translational research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ADAM10; Hepatocellular carcinoma; invasion; miR-449a; proliferation.
Affiliations: Department of Hepatobiliary and Pancreatic Surgery, The First Hospital, Jilin University Changchun, Jilin Province, China.

Abstract:  MicroRNAs (miRNAs) are a class of small, non-coding RNAs that play a crucial role in tumor procession. It has been demonstrated that miR-449a expression was downregulated and served as tumor suppressor in many types of tumor. However, the biological function and molecular mechanism of miR-449a in hepatocellular carcinoma (HCC) still remains largely unknown. Therefore, the aims of this study were to investigate biological role and molecular mechanism of miR-449a in HCC by a serial of molecular experiments. Here, we demonstrated that miR-449a expression was downregulated in HCC tissues and cell lines compared with the adjacent nontumor tissues and normal hepatic cell line. Ectopic expression of miR-449a suppressed HCC cell proliferation, colony formation, migration and invasion. Moreover, A Disintegrin And Metalloproteinases 10 (ADAM10) was identified as a direct target gene of miR-449a in HCC cell. ADAM10 expression was upregulated in HCC tissues and cell lines, and was negatively correlated with the expression level of miR-449a in HCC tissues. Interesting, overexpression of ADAM10 attenuated the inhibition effect of miR-449a-mediated HCC cell proliferation, colony formation, migration and invasion. These results suggested that miR-449a might function as a tumor suppressor miRNA, at least in part, through regulating ADAM10 expression in HCC. 

Retracted: Yes

PubPeer comments:
 Supplemental Fig. 7B u2013 A splicing is observed in Tor1 and Nop1, but not at Pgk, Pdi1 or Tim23 lanes. Could authors provide an explanation? ![file] ,
Disruption of mouse Cenpj, a regulator of centriole biogenesis, phenocopies Seckel syndrome
Authors: Darren W Logan
Fengtang Yang
Jeanne Estabel
Sanger Mouse Genetics Project
Ozama Ismail
Gabriela Sanchez-Andrade
Beiyuan Fu
Louise van der Weyden
Cheryl L Scudamore
Mark J Arends
Pavithra Lakshminarasimhan Chavali
Jacqueline K White
Stephen P Jackson
Damian M Carragher
Rebecca E McIntyre
Josep V Forment
Ferdia A Gallagher
David J Adams
Andrew Edwards
Martin Del Castillo Velasco-Herrera
Vinit B Mahajan
Ramiro Ramirez-Solis
Stephen H Tsang
Fanni Gergely
Journal: PLoS genetics (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CENPJ; Seckel syndrome; microcephaly; dwarfism; genomic instability
Affiliations: Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, United Kingdom.

Abstract:  Disruption of the centromere protein J gene, CENPJ (CPAP, MCPH6, SCKL4), which is a highly conserved and ubiquitiously expressed centrosomal protein, has been associated with primary microcephaly and the microcephalic primordial dwarfism disorder Seckel syndrome. The mechanism by which disruption of CENPJ causes the proportionate, primordial growth failure that is characteristic of Seckel syndrome is unknown. By generating a hypomorphic allele of Cenpj, we have developed a mouse (Cenpj(tm/tm)) that recapitulates many of the clinical features of Seckel syndrome, including intrauterine dwarfism, microcephaly with memory impairment, ossification defects, and ocular and skeletal abnormalities, thus providing clear confirmation that specific mutations of CENPJ can cause Seckel syndrome. Immunohistochemistry revealed increased levels of DNA damage and apoptosis throughout Cenpj(tm/tm) embryos and adult mice showed an elevated frequency of micronucleus induction, suggesting that Cenpj-deficiency results in genomic instability. Notably, however, genomic instability was not the result of defective ATR-dependent DNA damage signaling, as is the case for the majority of genes associated with Seckel syndrome. Instead, Cenpj(tm/tm) embryonic fibroblasts exhibited irregular centriole and centrosome numbers and mono- and multipolar spindles, and many were near-tetraploid with numerical and structural chromosomal abnormalities when compared to passage-matched wild-type cells. Increased cell death due to mitotic failure during embryonic development is likely to contribute to the proportionate dwarfism that is associated with CENPJ-Seckel syndrome. 

Retracted: No

PubPeer comments:
 ![file] , 
 This is clearly the same blot probed with multiple antibodies in fig1 and fig 5 so the KAP1 loading control is the same as expected. The other blots arenu2019t the same. ,
RETRACTED ARTICLE: p62 improves AD-like pathology by increasing autophagy
Authors: A Caccamo
C Branca
E Ferreira
S Oddo
Journal: Molecular Psychiatry (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: p62; neurodegenerative disorders; Alzheimer's disease; tau degradation; amyloid-β
Affiliations: The Arizona State University-Banner Neurodegenerative Disease Research Center, Biodesign Institute at Arizona State University, Tempe, AZ, USA., School of Life Sciences, Arizona State University, Tempe, AZ, USA.

Abstract:  The multifunctional protein p62 is associated with neuropathological inclusions in several neurodegenerative disorders, including frontotemporal lobar degeneration, amyotrophic lateral sclerosis and Alzheimer's disease (AD). Strong evidence shows that in AD, p62 immunoreactivity is associated with neurofibrillary tangles and is involved in tau degradation. However, it remains to be determined whether p62 also plays a role in regulating amyloid-β (Aβ) aggregation and degradation. Using a gene therapy approach, here we show that increasing brain p62 expression rescues cognitive deficits in APP/PS1 mice, a widely used animal model of AD. The cognitive improvement was associated with a decrease in Aβ levels and plaque load. Using complementary genetic and pharmacologic approaches, we found that the p62-mediated changes in Aβ were due to an increase in autophagy. To this end, we showed that removing the LC3-interacting region of p62, which facilitates p62-mediated selective autophagy, or blocking autophagy with a pharmacological inhibitor, was sufficient to prevent the decrease in Aβ. Overall, we believe these data provide the first direct in vivo evidence showing that p62 regulates Aβ turnover. 

Retracted: Yes

PubPeer comments:
 Fig.2D: According to figure legend, the mice number is 7, right? Could authors explain how to get 50% survival rate point (red arrow) and approximate 40% rate point (blue arrow, which 3 7(42.8%) but 4 7(57.1%) ) in March3- - group? ![image] , 
 I am Heng Lin, the first author of this paper. Upon your comment, we went over our original data and found that we made a mistake in using Graphpad Prism to analyze the survival data. The corrected figure is as following. We also made an error in the legend about the numbers of the mice. N=8 for wild-type mice, N=7 for the KO mice. The conclusion of this figure is not affected. ![file] , 
 #1 I am Heng Lin, the first author of this paper. Upon your comment, we went over our original data and found that we made a mistake in using Graphpad Prism to analyze the survival data. The corrected figure is as following. We also made an error in the legend about the numbers of the mice. N=8 for wild-type mice, N=7 for the KO mice. The conclusion of this figure is not affected. ![file] ,
Retracted : Antiproliferative Efficacy of Hesperetin (Citrus Flavanoid) in 1,2‐Dimethylhydrazine‐Induced Colon Cancer
Authors: Selvaraj Aranganathan
Namasivayam Nalini
Journal: Phytotherapy Research (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: AgNORs; PCNA; aberrant crypt foci; antiproliferation; colon cancer
Affiliations: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar--608002, Tamilnadu, India., Department of Biochemistry and Biotechnology Annamalai University  Annamalainagar 608 002 Tamilnadu India

Abstract:  Cancer is the second leading cause of death worldwide and is increasing at an alarming rate. The present study was to evaluate the antiproliferative effects of hesperetin, a flavonoid commonly found in many herbal medicines and foods, on aberrant crypt foci (ACF), argyrophylic nucleolar organizer regions (AgNORs) and proliferating cell nuclear antigen (PCNA) in 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats. Rats were given subcutaneous injections of DMH (20 mg/kg body weight) weekly for 15 weeks to induce carcinogenesis, and hesperetin was administered orally at the dose of 20 mg/kg body weight. DMH exposure alone produced a high incidence of ACF and showed positive staining for PCNA and AgNORs in colonic tissues. Supplementation with hesperetin lowered the PCNA labeling index and suppressed the formation of ACF in the rats with colon cancer. These results clearly reveal that dietary hesperetin possesses antiproliferative ability against chemically induced colon tumourigenesis. 

Retracted: Yes

PubPeer comments:
 The authors report that  Vitilinexu00ae bio-actives are an effective treatment of vitiligo, both in isolation and in combination with phototherapy. We read in a footnote that  The authors have declared that no competing interests exist . However, a little scrutiny reveals that Vitilinexu00ae bio-actives are produced and sold by the company Vitiligo.Clinicu00ae , described on [its website] as  a partnership between three of the world leading Professors in Dermatology: Professor **Torello Lotti**, Professor Davinder Parsad and Professor **Michael Tirant** . That is to say, the main author and the antepenultimate author. ![file] ![file] The claim that  no conflicting interests exist is absurd. In another cause for concern, there is nothing in the paper to indicate that the recipients of the herbal treatment gave consent for photographs of their body-parts to be used in this advertisement. Curious minds are wondering whether these  Vitilinex products are the same as the products previously sold directly branded with the Vitiligo.Clinic title, but that may be outside the scope of post-publication review. ![file] ,
miR-30d inhibits cell biological progression of Ewing's sarcoma by suppressing the MEK/ERK and PI3K/Akt pathways inï¿½vitro
Authors: Conglin Ye
Bin Zhang
Min Dai
Xuqiang Liu
Xiaolong Yu
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: Ewing's sarcoma; apoptosis; invasion and migration; microRNA-30d; mitogen-activated protein kinase kinase/extracellular signal-regulated kinase
Affiliations: Department of Orthopedics, The First Affiliated Hospital of Nanchang University, Artificial Joints Engineering and Technology Research Center of Jiangxi Province, Nanchang, Jiangxi 330006, P.R. China.

Abstract:  MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules involved in cancer initiation and progression. The present study aimed to determine the effect of miRNA-30d (miR-30d) on the growth, malignant phenotype, and apoptosis of Ewing's sarcoma (ES) SK-ES-1 cells, and to elucidate the underlying molecular mechanism and signaling pathway involved. Cell proliferation, invasion, migration, morphological changes, cell cycle distribution and apoptosis were investigated. Furthermore, the expression of matrix metalloproteinase (MMP)-2, MMP-9, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and poly (ADP-ribose) polymerase (PARP) were examined, as was the activity of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/Akt pathways. It was found that the overexpression of miR-30d repressed the proliferation, migration and invasion, and promoted morphological changes, S-phase arrest and apoptosis of SK-ES-1 cells. Additionally, it was observed that increased miR-30d levels inhibited the expression of MMP-2 and MMP-9, and inhibited the activity of the MEK/ERK and PI3K/Akt pathways, but elevated the ratio of Bax/Bcl-2 and the cleavage of caspase-3 and PARP. Taken together, the results demonstrated that miR-30d suppressed the biological progression of SK-ES-1 cells by targeting MMP-2 and MMP9, the Bax/Bcl-2 and caspase-3 cascade, and the MEK/ERK and PI3K/Akt signaling pathways. Therefore, miR-30d is a promising target in the treatment of ES. However, further investigations are urgently required to investigate the underlying molecular mechanisms of the effects of miR-30d on ES for a comprehensive understanding of the tumorigenesis and progression of this cancer. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 **Additional DUPLICATION be the same authors!** ![file] , 
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 ![file] ,
The preparation of a novel iron/manganese binary oxide for the efficient removal of hexavalent chromium [Cr(vi)] from aqueous solutions
Authors: Feng Dang
Cheng Yang
Haojie Lv
Xiaoning Wang
Xifeng Shi
Yuqi Fan
Chuanxi Yang
Weiliang Wang
Tiantian Ju
Yujia Ji
Wenping Dong
Ying Wang
Journal: RSC Advances (2020)
Discipline: CHEMISTRY
Keywords: Fe-Mn binary oxide; adsorbent preparation; Cr(vi) removal; characterization; adsorption capacity
Affiliations: Institute of Environment and Ecology, Shandong Normal University, Jinan 250358, China, College of Resources and Environmental Sciences, Construction Project Environmental Assessment Service Center of Shandong Province, Jinan 250012, School of Mechanical Engineering and Automation, Northeastern University, Shenyang 110819, College of Art and Science, University of Vermont, Burlington, USA, School of Physics and Electronics, Jinan 250014, Shandong Academy of Environmental Science Co., Ltd., Jinan 250013, Key Laboratory for Liquid-Solid Structural Evolution and Processing of Materials, Shandong University, Jinan 250061, College of Chemistry, Chemical Engineering and Materials Science, College of Geography and Environment

Abstract:  To remove hexavalent chromium Cr(vi) efficiently, a novel Fe-Mn binary oxide adsorbent was prepared via a "two-step method" combined with a co-precipitation method and hydrothermal method. The as-prepared Fe-Mn binary oxide absorbent was characterized via transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray diffraction (XRD), Fourier-transform infrared spectra (FTIR), thermogravimetric analysis (TGA), zeta potential, BET and X-ray photoelectron spectroscopy (XPS). The results indicated that the morphology of the adsorbent was rod-like with length of about 100 nm and width of about 50-60 nm, specific surface area was 63.297 m2 g-1, has the composition of α-Fe2O3, β-MnO2 and MnFe2O4 and isoelectric point was observed at pH value of 4.81. The removal of Cr(vi) was chosen as a model reaction to evaluate the adsorption capacity of the Fe-Mn binary oxide adsorbent, indicating that the Fe-Mn binary oxide adsorbent showed high adsorption performance (removal rate = 99%) and excellent adsorption stability (removal rate &gt; 90% after six rounds of adsorption). The adsorption behavior of the Fe-Mn binary oxide was better represented by the Freundlich model (adsorption isotherm) and the pseudo-second-order model (adsorption kinetic), suggesting that the adsorption process was multi-molecular layer chemical adsorption. The possible adsorption mechanism of the Fe-Mn binary oxide for the removal of Cr(vi) included the protonation process and the electrostatic attraction interactions. 

Retracted: No

PubPeer comments:
 Fig 1G. There is no obvious difference among the three central panels, or between the far-left and far-right panels, except at the highest levels of PI-A, and for the different curves fitted to the data. ![file] ,
Galectin-3 gene silencing inhibits migration and invasion of human tongue cancer cells in vitro via downregulating β-catenin
Authors: Feng-cai Wei
Zuo-qing Dong
Dong Zhang
Martin Dalin
Zheng-gang Chen
Ying-wei Hu
Shi-san Bao
Shao-hua Liu
Journal: Acta Pharmacologica Sinica (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Galectin-3; tongue cancer; migration; invasion; β-catenin
Affiliations: Department of Oral Maxillofacial Surgery, Qilu Hospital, Shandong University, Ji-nan, China.

Abstract:  Aim: Galectin-3 (Gal-3) is a member of the carbohydrate-binding protein family that contributes to neoplastic transformation, tumor survival, angiogenesis, and metastasis. The aim of this study is to investigate the role of Gal-3 in human tongue cancer progression. Methods: Human tongue cancer cell lines (SCC-4 and CAL27) were transfected with a small-interfering RNA against Gal-3 (Gal-3-siRNA). The migration and invasion of the cells were examined using a scratch assay and BD BioCoat Matrigel Invasion Chamber, respectively. The mRNA and protein levels of β-catenin, Akt/pAkt, GSK-3β/pGSK-3β, MMP-9 in the cells were measured using RT-PCR and Western blotting, respectively. Results: Transient silencing of Gal-3 gene for 48 h significantly suppressed the migration and invasion of both SCC-4 and CAL27 cells. Silencing of Gal-3 gene significantly decreased the protein level of β-catenin, leaving the mRNA level of β-catenin unaffected. Furthermore, silencing Gal-3 gene significantly decreased the levels of phosphorylated Akt and GSK-3β, and suppressed the mRNA and protein levels of MMP-9 in the cells. Conclusion: Our data suggest that Gal-3 mediates the migration and invasion of tongue cancer cells in vitro via regulating the Wnt/β-catenin signaling pathway and Akt phosphorylation. 

Retracted: No

PubPeer comments:
 The DMSO panels in Figure 1C and 1D appear to look very similar, albeit with different gated percentages. Shown with red boxes. ![file] , 
 The Anti-miR-NC panels in Figure 4C and 4D appear to look very similar, albeit with different gated percentages. Shown with blue boxes. ![file] , 
 There is a gleaning mistake in the first few sentences of the article:  Morin (3,5,7,20,40-pentahydroxyflavone) is an anti-tumor flavonoid in a numerous types of cancer cells including breast, ovarian and lung cancers. A corrected version would read: Morin (3,5,7,2 ,4 -pentahydroxyflavone ) is an flavonoid with anti-cancer activity in numerous types of cancer cells including breast, ovarian and lung. ,
The prion organotypic slice culture assay--POSCA
Authors: Adriano Aguzzi
Jeppe Falsig
Journal: Nature Protocols (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: prion replication; ex vivo; prion strains; organotypic slice culture assay (POSCA); prion amplification
Affiliations: Institute of Neuropathology, Department of Pathology, University of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland.

Abstract:  Methods enabling prion replication ex vivo are important for advancing prion science. However, few such technologies exist and many prion strains are intractable with them. Here, we describe a prion organotypic slice culture assay (POSCA), which allows for prion amplification and titration ex vivo under conditions that closely resemble intracerebral infection. Organotypic slices are incubated with infectious inoculum as free-floating sections, washed and cultured for up to 8 weeks. Slice cultures are a rich source of protein or RNA and allow for stringent comparisons between uninfected and prion-infected samples generated from the same mouse. Thirty-five days after contact with prions, cerebellar slices have amplified PrP(Sc) quantitatively similar to that seen in vivo, but accelerated fivefold. The POSCA detects replication of specific prion strains from disparate sources, including bovines and ovines, with variable efficiency. The culture procedure and prion infection can be performed in 8 h. 

Retracted: No

PubPeer comments:
 Fig 3A.  Observation of ultrastructure of brain tissues of rats in each group by the TEM . ![file] How to explain the internal repetitions of one panel, or the 180-deg symmetry of one visual element? ![file] More internal repetitions in another panel. ![file] , 
 Fig 3C.  Observation of the pathological condition of brain tissues of rats in each group by Nissl staining . ![file] It is difficult to believe that these images are real-world observations. ![file] ,
Orientation-specific learning of the prior assumption for 3D slant perception
Authors: Masayuki Sato
Shuichiro Taya
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: Trapezoidal image; 3D slant; Shape prior; Perspective transformation; Stereoscopic reference plane
Affiliations: Keio University, 4-1-1, Hiyoshi, Kohoku-ku, Yokohama, 223-8521, Japan., The University of Kitakyushu, 1-1, Hibikino, Wakamatsu-ku, Kitakyushu, 808-0135, Japan. .

Abstract:  We usually interpret a trapezoidal image on our retina as a slanted rectangle rather than a frontoparallel trapezoid, because we use a statistical assumption (i.e. rectangles are more common than trapezoids), called a 'prior', for recovering the 3D world from ambiguous 2D images. Here we report that the shape prior for recovering 3D slant can be updated differently depending on the slant axis orientation (horizontal vs. vertical). The participants were exposed to a variety of trapezoidal images surrounded by a stereoscopic reference plane. The perspective transformation of the images was interpreted as 2D shape, rather than 3D slant because the surrounding plane enhanced disparity. We found that, after continuous exposure to such images, the participants relied less on the shape information for recovering 3D slant, suggesting the update of priors via experience (i.e., rectangles are less common than trapezoids). Importantly, the learning effect was context (slant-axis) specific although partially transferred across contexts; the training with horizontal-axis slant reduced the reliance on perspective even in vertical-axis slant estimation but not vice versa. The results suggest that context-specific training is vital to update the prior for the horizontal-axis slant, whereas it is not required to update the prior for a vertical-axis slant. 

Retracted: No

PubPeer comments:
 Figure 2c and d ![file] , 
 Color-reversing the Migration panels and superimposing them on the Invasion panels, the areas of cancellation (where images are identical) are impressively large. ![file] , 
 **Retracted** February 3, 2022 u201cWe, the Editors and Publisher of the journal Artificial Cells, Nanomedicine, and Biotechnology, have retracted the following article: Shaosong Huang, Shihao Zheng, Shengyue Huang, Hui Cheng, Ying Lin, Yuxing Wen Wei Lin (2019) Flot2 targeted by miR-449 acts as a prognostic biomarker in glioma. Artificial Cells, Nanomedicine, and Biotechnology, 47(1), 250u2013255, DOI: 10.1080 21691401.2018.1549062 Since publication, concerns have been raised about the integrity of the data in the article. When approached for an explanation, the authors have been unresponsive, and we have been unable to verify their original data. We are therefore retracting this article and the corresponding author listed in this publication has been informed. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. u201c ,
ZCCHC3 modulates TLR3-mediated signaling by promoting recruitment of TRIF to TLR3
Authors: Xuan Zhong
Hong-Bing Shu
Huan Lian
Qing Yang
Ru Zang
Journal: Journal of molecular cell biology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TLR3; TRIF; ZCCHC3; innate immune response; signaling.
Affiliations: Department of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.

Abstract:  Toll-like receptor 3 (TLR3)-mediated signaling is important for host defense against RNA virus. Upon viral RNA stimulation, toll and interleukin-1 receptor domain-containing adaptor inducing IFN-β (TRIF) is recruited to TLR3 and then undergoes oligomerization, which is required for the recruitment of downstream molecules to transmit signals. Here, we identified zinc finger CCHC-type containing 3 (ZCCHC3) as a positive regulator of TLR3-mediated signaling. Overexpression of ZCCHC3 promoted transcription of downstream antiviral genes stimulated by the synthetic TLR3 ligand poly(I:C). ZCCHC3-deficiency markedly inhibited TLR3- but not TLR4-mediated induction of type I interferons (IFNs) and proinflammatory cytokines. Zcchc3-/- mice were more resistant to poly(I:C)- but not lipopolysaccharide-induced inflammatory death. Mechanistically, ZCCHC3 promoted recruitment of TRIF to TLR3 after poly(I:C) stimulation. Our findings reveal that ZCCHC3 plays an important role in TLR3-mediated innate immune response by promoting the recruitment of TRIF to TLR3 after ligand stimulation. 

Retracted: No

PubPeer comments:
 In Figure 7c, a Western blot lane has been duplicated and presented as something else. ![file] ,
Modulation of nucleotide excision repair by mammalian SWI/SNF chromatin-remodeling complex
Authors: Qi-En Wang
Gulzar Wani
Keisha Milum
Qun Zhao
Alo Ray
Altaf A Wani
Chunhua Han
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Chromatin accessibility; Nucleotide excision repair (NER); SWI/SNF complex; Brg1; UV-induced DNA damage
Affiliations: Department of Radiology, The Ohio State University, Columbus, Ohio 43210, USA.

Abstract:  Accessibility within chromatin is an important factor in the prompt removal of UV-induced DNA damage by nucleotide excision repair (NER). Chromatin remodeling by the SWI/SNF complex has been shown to play an important modulating role in NER in vitro and yeast in vivo. Nevertheless, the molecular basis of cross-talk between SWI/SNF and NER in mammalian cells is not fully understood. Here, we show that knockdown of Brg1, the ATPase subunit of SWI/SNF, negatively affects the elimination of cyclobutane pyrimidine dimers (CPD), but not of pyrimidine (6, 4)pyrimidone photoproducts (6-4PP) following UV irradiation of mammalian cells. Brg1-deficient cells exhibit a lower chromatin relaxation as well as impaired recruitment of downstream NER factors, XPG and PCNA, to UV lesions. However, the assembly of upstream NER factors, DDB2 and XPC, at the damage site was unaffected by Brg1 knockdown. Interestingly, Brg1 interacts with XPC within chromatin and is recruited to UV-damaged sites in a DDB2- and XPC-dependent manner. Also, postirradiation decrease of XPC levels occurred more rapidly in Brg1-deficient than normal cells. Conversely, XPC transcription remained unaltered upon Brg1 knockdown indicating that Brg1 affects the stability of XPC protein following irradiation. Thus, Brg1 facilitates different stages of NER by initially modulating UV-induced chromatin relaxation and stabilizing XPC at the damage sites, and subsequently stimulating the recruitment of XPG and PCNA to successfully culminate the repair. 

Retracted: No

PubPeer comments:
 ![file] , 
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