PReD-Bench/PRed-Bench huggingface dataset:
MicroRNA-212 targets FOXA1 and suppresses the proliferation and invasion of intrahepatic cholangiocarcinoma cells
Authors: Hongbo Xu
Lei Zhu
Zhongjie Yi
Shaopeng Zheng
Feizhou Huang
Tao Wan
Gang Deng
Wanpin Nie
Wei Huang
Journal: Experimental and Therapeutic Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: Retraction; Article; DOI; Research; Abstract

Abstract:  [This retracts the article DOI: 10.3892/etm.2016.3824.]. 

Retracted: No

PubPeer comments:
 Retracted [10 March 2017] . ----------------------------- We wish to retract our research article entitled u201cMicroRNA-212 targets FOXA1 and suppresses the proliferation and invasion of intrahepatic cholangiocarcinoma cellsu201d, published in Experimental and Therapeutic Medicine 12: 3790-3796, 2016. We have discovered that some important data from the in vitro experiments was inadvertently omitted when we performed the statistical analysis, and this may consequently have affected the results of that analysis. As a result, we wish to retract this article so that the manuscript may be suitably revised. All the named authors on the paper agree to this retraction. We sincerely apologize for any inconvenience that might result from the retraction of this article. ----------------------------------------- Fig 3.  Transwell assays were conducted to assess the invasion of intrahepatic cholangiocarcinoma QBC939 cells transfected with miR-212 mimics or miR-NC. Non-transfected QBC939 cells were used as a control . ![file] For comparison, Fig 3 C D from [Zhang et al (2016)] .  Transwell assay were performed to examine the migratory and invasive capacities of Saos-2 and U2OS cells transfected with miR-205 mimic or miR-negative control (NC) mimic , and Fig 7C D,  Transwell assay were performed to examine cell migration and invasion of MG63 or U2OS cells transfected with miR-205 mimic, or co-transfected with miR-205 mimic and RUNX2 plasmid . ![] Colored rectangles mark similar panels in Figs 2(C) and 4(C) of [Jiao et al (2016)] . ![file] Some other manifestations of these versatile panels are linked in those threads. ,
Long non-coding RNA activated by transforming growth factor beta alleviates lipopolysaccharide-induced inflammatory injury via regulating microRNA-223 in ATDC5 cells
Authors: Qiao Zhang
Hongliang Ying
Yongkun Wang
Zhongwen Gao
Journal: International immunopharmacology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Inflammatory injury; Long non-coding RNA-activated by transforming growth factor beta (lncRNA-ATB); MicroRNA-223; MyD88/NF-κB; Osteoarthritis
Affiliations: Department of Orthopaedics, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China., Department of Orthopaedics, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. Electronic address: .

Abstract:  Osteoarthritis (OA) is a conversant joint disease, which seriously threatens the health of the elderly, and even leads to disability. Long non-coding RNA-activated by transforming growth factor beta (lncRNA-ATB) has been reported in diverse cancers. However, the functions of lncRNA-ATB in OA remain uninvestigated. The current study aimed to explore the impacts of lncRNA-ATB on lipopolysaccharide (LPS)-induced inflammatory injury in ATDC5 cells and to uncover the underlying mechanism. LPS-induced ATDC5 cell injury model was constructed, and the effects of lncRNA-ATB on LPS-injured cells were explored via analyzing cell viability, apoptosis, iNOS, COX-2, and inflammatory cytokines (IL-6 and TNF-α). Subsequently, the relationship between lncRNA-ATB and microRNA (miR)-223 was detected, and whether miR-223 was involved in modulating LPS-induced cells injury in ATDC5 cells was investigated. Finally, MyD88/NF-κB and p38MAPK pathways were assessed to explore the underlying mechanism. Results showed that LPS repressed cell viability, induced apoptosis, and promoted iNOS, COX-2, IL-6 and TNF-α expression. Additionally, we observed that lncRNA-ATB expression was down-regulated in LPS-injured cells, and lncRNA-ATB overexpression significantly alleviated LPS-induced inflammatory injury in ATDC5 cells. Interesting results revealed that miR-223 expression was down-regulated by lncRNA-ATB and miR-223 overexpression declined the protective effect of lncRNA-ATB on LPS-injured ATDC5 cells. Further, the signaling pathway experiments showed that lncRNA-ATB inhibited MyD88/NF-κB and p38MAPK pathways by down-regulating miR-223 in LPS-injured cells. These data demonstrated that lncRNA-ATB protected ATDC5 cells against LPS-induced inflammatory injury by repressing MyD88/NF-κB and p38MAPK pathways, which was mediated by down-regulation of miR-223. 

Retracted: No

PubPeer comments:
 The in vivo study part is useless Bacterial load comparisons are impossible because treatment with maltodextrin group has higher organic carbon intake than control group, additional control group with glucose in drinking water would have been more informative and allowed for direct comparison between bacterial loads ,
12/15-Lipoxygenase Inhibition Reverses Cognitive Impairment, Brain Amyloidosis, and Tau Pathology by Stimulating Autophagy in Aged Triple Transgenic Mice
Authors: Domenico Praticò
Elisabetta Lauretti
Magid Abou-Gharbia
Jian-Guo Li
Benjamin E Blass
Antonio Di Meco
Journal: Biological psychiatry (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: 12/15-Lipoxygenase; Alzheimer’s disease; Amyloid beta; Animal model; Autophagy
Affiliations: Center for Translational Medicine, Lewis Katz School of Medicine, Philadelphia, Pennsylvania., The Moulder Center for Drug Discovery Research, Temple University School of Pharmacy, Philadelphia, Pennsylvania., Center for Translational Medicine, Lewis Katz School of Medicine, Philadelphia, Pennsylvania. Electronic address: .

Abstract:  Background: The 12/15-lipoxygenase (12/15-LO) enzyme is upregulated in the brains of patients with Alzheimer's disease (AD), and its expression levels influence the onset of the AD-like phenotype in mouse models. However, whether targeting this pathway after the neuropathology and behavioral impairments have been established remains to be investigated. Methods: Triple transgenic (3xTg) mice received either PD146176-a selective and specific pharmacological inhibitor of 12/15-LO-or placebo starting at 12 months of age for 12 weeks. They were then assessed for the effect of the treatment on neuropathologies and behavioral impairments. Results: At the end of the study, mice in the control group showed a worsening of memory and learning abilities, whereas mice receiving PD146176 were undistinguishable from wild-type mice. The same group also had significantly lower amyloid beta levels and deposition, less tau neuropathology, increased synaptic integrity, and autophagy activation. Ex vivo and in vitro genetic and pharmacological studies found that the mechanism involved in these effects was the activation of neuronal autophagy. Conclusions: Our findings provide new insights into the disease-modifying action of 12/15-LO pharmacological inhibition and establish it as a viable therapeutic approach for patients with AD. 

Retracted: No

PubPeer comments:
 **Figure 3E**: The actin blots seem too similar to be from different sets of mice, as stated in the caption. ![file] In false colors: ![file] Part of the caption relative to the 3E image: ![file] ,
Loss of inhibitory semaphorin 3A (SEMA3A) autocrine loops in bone marrow endothelial cells of patients with multiple myeloma
Authors: Franco Dammacco
Guido Serini
Angelo Vacca
Francesca Merchionne
Andrea Bacigalupo
Teresa Cirulli
Giovanna Piaggio
Giulia Di Pietro
Diego Guidolin
Domenico Ribatti
Claudio Scavelli
Federico Bussolino
Journal: Blood (2006)
Discipline: CLINICAL MEDICINE
Keywords: VEGF165; SEMA3A; angiogenic potential; endothelial cells; MM
Affiliations: From the Department of Internal Medicine and Clinical Oncology and the Department of Human Anatomy and Histology, University of Bari Medical School, Bari; the Department of Oncological Sciences and Division of Molecular Angiogenesis, Institute for Cancer Research and Treatment, University of Turin Medical School, Candiolo; the Department of Human Anatomy and Physiology, University of Padua Medical School, Padua; and the Department of Hemato-Oncology, S Martino Hospital, Genoa, Italy.

Abstract:  Vascular endothelial growth factor165 (VEGF165) and semaphorin3A (SEMA3A) elicit pro- and antiangiogenic signals respectively in endothelial cells (ECs) by binding to their receptors VEGFR-2, neuropilin-1 (NRP1), and plexin-A1. Here we show that the VEGF165-driven angiogenic potential of multiple myeloma (MM) ECs is significantly higher than that of monoclonal gammopathy of undetermined significance (MGUS) ECs (MGECs) and human umbilical vein (HUV) ECs. This is probably due to a constitutive imbalance of endogenous VEGF165/SEMA3A ratio, which leans on VEGF165 in MMECs but on SEMA3A in MGECs and HUVECs. Exogenous VEGF165 induces SEMA3A expression in MGECs and HUVECs, but not in MMECs. Moreover, by counteracting VEGF165 activity as efficiently as an anti-VEGFR-2 antibody, exogenous SEMA3A restrains the over-angiogenic potential of MMECs. Our data indicate that loss of endothelial SEMA3A in favor of VEGF165 could be responsible for the angiogenic switch from MGUS to MM. 

Retracted: No

PubPeer comments:
 Figure 4. Much more similar than you would expect. https: imgur.com t82gnUQ ,
Effective inhibition of foot-and-mouth disease virus (FMDV) replication in vitro by vector-delivered microRNAs targeting the 3D gene
Authors: Xuepeng Cai
Guozheng Cong
Guofeng Zhang
Huiyun Chang
Shandian Gao
Junjun Shao
Tong Lin
Junzheng Du
Jihuai Luo
Journal: Virology Journal (2011)
Discipline: MICROBIOLOGY
Keywords: Foot-and-mouth disease virus; FMDV; miRNA; siRNA; RNAi
Affiliations: State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, China.

Abstract:  Background: Foot-and-mouth disease virus (FMDV) causes an economically important and highly contagious disease of cloven-hoofed animals. RNAi triggered by small RNA molecules, including siRNAs and miRNAs, offers a new approach for controlling viral infections. There is no report available for FMDV inhibition by vector-delivered miRNA, although miRNA is believed to have more potential than siRNA. In this study, the inhibitory effects of vector-delivered miRNAs targeting the 3D gene on FMDV replication were examined. Results: Four pairs of oligonucleotides encoding 3D-specific miRNA of FMDV were designed and selected for construction of miRNA expression plasmids. In the reporter assays, two of four miRNA expression plasmids were able to significantly silence the expression of 3D-GFP fusion proteins from the reporter plasmid, p3D-GFP, which was cotransfected with each miRNA expression plasmid. After detecting the silencing effects of the reporter genes, the inhibitory effects of FMDV replication were determined in the miRNA expression plasmid-transfected and FMDV-infected cells. Virus titration and real-time RT-PCR assays showed that the p3D715-miR and p3D983-miR plasmids were able to potently inhibit the replication of FMDV when BHK-21 cells were infected with FMDV. Conclusion: Our results indicated that vector-delivered miRNAs targeting the 3D gene efficiently inhibits FMDV replication in vitro. This finding provides evidence that miRNAs could be used as a potential tool against FMDV infection. 

Retracted: No

PubPeer comments:
 image duplications ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. , 
 One additional concern in orange. Note that some of these images have been resized. *** ![file] ,
Downregulation of MCT1 inhibits tumor growth, metastasis and enhances chemotherapeutic efficacy in osteosarcoma through regulation of the NF-κB pathway
Authors: Dawei Liu
Jingnan Shen
Tiebang Kang
Junqiang Yin
Changye Zou
Qinglian Tang
Jinchang Lu
Jin Wang
Yuanzhong Wu
Man-Si Wu
Zhiqiang Zhao
Xianbiao Xie
Journal: Cancer Letters (2014)
Discipline: CLINICAL MEDICINE
Keywords: CHC; MCT1; NF-κB pathway; Osteosarcoma.
Affiliations: Department of Musculoskeletal Oncology, First Afflicted Hospital, Sun Yat-Sen University, Guangzhou 510080, China.

Abstract:  Monocarboxylate transporter isoform 1 (MCT1) is an important member of the proton-linked MCT family and has been reported in an array of human cancer cell lines and primary human tumors. MCT1 expression is associated with developing a new therapeutic approach for cancer. In this study, we initially showed that MCT1 is expressed in a variety of human osteosarcoma cell lines. Moreover, we evaluated the therapeutic response of targeting MCT1 using shRNA or MCT1 inhibitor. Inhibiting MCT1 delayed tumor growth in vitro and in vivo, including in an orthotopic model of osteosarcoma. Targeting MCT1 greatly enhanced the sensitivity of human osteosarcoma cells to the chemotherapeutic drugs adriamycin (ADM). In addition, we observed that MCT1 knockdown significantly suppressed the metastatic activity of osteosarcoma, including wound healing, invasion and migration. Further mechanistic studies revealed that the antitumor effects of targeting MCT1 might be related to the NF-κB pathway. Immunochemistry assay showed that MCT1 was an independent positive prognostic marker in osteosarcoma patients. In conclusion, our data, for the first time, demonstrate that MCT1 inhibition has antitumor potential which is associated with the NF-κB pathway, and high MCT1 expression predicates poor overall survival in patients with osteosarcoma. 

Retracted: No

PubPeer comments:
 Fig. 4a and Fig. 4b contain two sets of overlapped images. ![file] ,
Agmatine Protects Against 6-OHDA-Induced Apoptosis, and ERK and Akt/GSK Disruption in SH-SY5Y Cells
Authors: Rasoul Ghasemi
Maryam Moosavi
Esmat Amiri
Journal: Cellular and Molecular Neurobiology (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: 6-OHDA; Akt; Caspase-3; ERK; GSK-3β
Affiliations: Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran., Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran., Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran., Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran. ., Nanotechnology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. .

Abstract:  6-Hydroxydopamine (6-OHDA), a metabolite of dopamine is known to induce dopaminergic cell toxicity which makes that a suitable agent inducing an experimental model of Parkinson's disease (PD). Agmatine has been shown to protect against some cellular and animal PD models. This study was aimed to assess whether agmatine prevents 6-OHDA-induced SH-SY5Y cell death and if yes, then how it affects Akt/glycogen synthesis kinase-3β (GSK-3β) and extracellular signal-regulated kinases (ERK) signals. The cells were treated with different drugs, and their viability was examined via MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay and morphological observation. Western blot studies were done to assess cleaved caspase-3, Akt/GSK-3β, and ERK proteins. 6-OHDA-induced cell death and caspase-3 cleavage, while agmatine prevented those changes. 6-OHDA also decreased the amount of phosphorylated Akt (pAkt)/Akt while increased GSK-3β activity which was prevented by agmatine. Additionally, this toxin increased pERK/ERK ratio which was averted again by agmatine. The PI3/Akt inhibitor, LY294002, impeded the changes induced by agmatine, while ERK inhibitor (PD98059) did not disturb the effects of agmatine, and by itself, it preserved the cells against 6-OHDA toxicity. This study revealed that agmatine is protective in 6-OHDA model of PD and affects Akt/GSK-3β and ERK pathways. 

Retracted: No

PubPeer comments:
 OMCIJ = 10.19080 omcij.2018.06.555677 https: www.pubpeer.com publications EC10E8546D7095D9B06CD780ACF461 GII = 10.15761 GII.1000153 https: www.pubpeer.com publications F803C559A989E1DA43211345F81122 These are essentially duplicate publications. Figure 1 is shown for comparison: https: imgur.com a fwuujSY ,
Nose size indicates maximum penile length
Authors: Haruki Kume
Yusuke Sato
Tadaichi Kitamura
Hiroshi Ikegaya
Motofumi Suzuki
Hiroki Kondou
Taketo Kawai
Journal: Basic and Clinical Andrology (2021)
Discipline: CLINICAL MEDICINE
Keywords: Aging; Cadaver; Nose size; Stretched penile length.
Affiliations: Department of Forensics Medicine, Graduate School of Medicine, Kyoto Prefectural University of Medicine, Kajii-cho 465, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan. ., Department of Urology, Tokyo Metropolitan Bokutoh Hospital, 4-23-15 Kotobashi, Sumida-ku, Tokyo, 130-8575, Japan., Department of Urology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan., Department of Forensics Medicine, Graduate School of Medicine, Kyoto Prefectural University of Medicine, Kajii-cho 465, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.

Abstract:  Background: In a previous report, we investigated whether the size of male genitalia similarly exposed to serum testosterone during aging could change with age and found that penile length almost stopped increasing during adolescence and decreased in older males. In this report, to determine what factors other than age are related to penile length, we performed a multivariate analysis of the relationships between stretched penile length (SPL) and other measurements of genital organs, nose size, height and body weight in 126 adults in their 30s-50s. Results: The most highly correlated factor with SPL was flaccid penile length (r = 0.565, P &lt; 0.0001). The next highest correlation was nose size (r = 0.564, P &lt; 0.0001). The penile stretched rate correlated with FPL (r = - 0.690, P &lt; 0.0001) but not with SPL or penile circumference. Conclusions: The fact that nose size is related to SPL indicates that penile length may not be determined by age, height or body weight but has already been determined before birth. 

Retracted: No

PubPeer comments:
  One hundred twenty-six male forensic autopsy cases at Kyoto Prefectural University of Medicine from April 2015 to March 2019 were used in this study. All cases were in their 30su201350s, and their postmortem time was within 3 days. Why were dead subjects used, and not living ones?  Consent for publication Informed consent was obtained from legal guardians. Were the  legal guardians explicitly aware that the penis of their dead relatives was going to be pulled or stretched in this manner? Incidentally, massive media attention: https: bacandrology.biomedcentral.com articles 10.1186 s12610-021-00121-z metrics ,
Inhibition effects of acridone on the growth of breast cancer cells in vivo
Authors: Y-F Xia
G-J Jiang
Y-C Che
H-J Chu
G-F Kuang
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: acridone; breast cancer; tumor inhibition; nude mice; xenografted tumor model
Affiliations: Department of Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, China. .

Abstract:  Objective: To investigate the anti-tumor effect of acridone against breast cancer in vivo and provide a therapeutic agent for treatment of breast cancer. Materials and methods: The nude mice xenografted tumor model was established by MCF-7 cells. The mice were randomly divided into four groups. The mice in each group (n=6) were intraperitoneally injected with 0.1 mg/kg saline (low-dose), 0.5 mg/kg (middle-dose) and 1.0 mg/kg (high-dose) of acridone for 21 days, respectively. At the end of the animal experiment, the weight of tumors was recorded to calculate the tumor inhibition rate. The serum hormone levels in peripheral blood were determined using ELISA. Hematoxylin and eosin (HE) staining was used to analyze the histopathological changes. The expression of ABCG2 protein and mRNA were determined by Western blot and RT-PCR, respectively. Results: The inhibition rates of tumor growth in the high-dose, middle-dose, and low-dose groups were 29.18%, 17.21%, and 4.27%, respectively. Compared with control and low-dose group, the tumors growth rate in high-dose and middle-dose groups were decreased significantly. Histologically, the tumors were inhibited in the growth rate, the tissue structure was broken. Estrogen in all groups with acridone treatment decreased, the progesterone in high-dose and middle-dose groups increased remarkably. The expression of ABCG2 protein and ABCG2 mRNA decreased after treatment with acridone. Conclusions: We showed that acridone could induce cell apoptosis, inhibited ABCG2 (ATP-binding cassette sub-family G member 2) protein and adjusted hormone level. The results suggested that acridone could serve as a chemotherapeutic agent for treatment of breast cancer in vivo. 

Retracted: No

PubPeer comments:
 Figure 2. * Red boxes: Two panels appear to show an overlap. ![file] ,
The role of PARP inhibition in triple-negative breast cancer: Unraveling the wide spectrum of synthetic lethality
Authors: Giannis Mountzios
Marios Papadimitriou
Christos A Papadimitriou
Journal: Cancer Treatment Reviews (2018)
Discipline: CLINICAL MEDICINE
Keywords: Homologous recombination; PARP; PARP inhibitors; Synthetic lethality; Triple negative breast cancer.
Affiliations: Second Department of Surgery, Aretaieion University Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece. Electronic address: ., Department of Medical Oncology, 251 Airforce General Hospital, Athens, Greece., Second Department of Surgery, Aretaieion University Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece.

Abstract:  Triple-negative breast cancer (TNBC) accounts for approximately 15-20% of all breast cancers and is characterized by a lack of immunohistochemical expression of estrogen receptors (ER), progesterone receptors (PR) and HER2. TNBC is associated with poor long-term outcomes compared with other breast cancer subtypes. Many of these tumors are also basal-like cancers which are characterized by an aggressive biological behavior with a distant recurrence peak observed early at 3 years following diagnosis. Furthermore, metastatic TNBC bears a dismal prognosis with an average survival of 12 months. Although the prevalence of genetic alterations among women with TNBC differs significantly by ethnicity, race and age, BRCA mutations (including both germline mutations and somatic genetic aberrations) are found in up to 20-25% of unselected patients and especially in those of the basal-like immunophenotype. Therefore, defects in the DNA repair pathway could represent a promising therapeutic target for this subgroup of TNBC patients. Poly(ADP-ribose) polymerase (PARP) inhibitors exploit this deficiency through synthetic lethality and have emerged as promising anticancer therapies, especially in BRCA1 or BRCA2 mutation carriers. Several PARP inhibitors are currently being evaluated in the adjuvant, neo-adjuvant, and metastatic setting for the treatment of breast cancer patients with a deficient homologous recombination pathway. In this article, we review the major molecular characteristics of TNBC, the mechanisms of homologous recombination, and the role of PARP inhibition as an emerging therapeutic strategy. 

Retracted: No

PubPeer comments:
 When you read a review article, you expect that the authors have the necessary knowledge and convey the correct information. The authors are obviously not updated in the PARP inhibition field. They use Iniparib as an example of an PARP inhibitor, but Iniparib is not a PARP inhibitor. This was clearly described in 2012: https: clincancerres.aacrjournals.org content 18 2 510 https: clincancerres.aacrjournals.org content 18 6 1655 ,
Gastrointestinal Foxp3 expression in normal, inflammatory and neoplastic conditions
Authors: Elisabetta Antonelli
Tarcisio Not
Gabrio Bassotti
Alberto Tommasini
Riccardo Nascimbeni
Fortunato Ferrara
Vincenzo Villanacci
Stefania Manenti
Journal: Pathology (2011)
Discipline: CLINICAL MEDICINE
Keywords: Foxp3; regulatory T lymphocytes; gastrointestinal tract; inflammatory conditions; preneoplastic conditions
Affiliations: Department of Pathology, Spedali Civili, Brescia, Italy. 

Abstract:  Background: Foxp3(+) regulatory T lymphocytes (T-regs) represent an important regulatory cell subset in inflammatory, preneoplastic and neoplastic conditions of the gastrointestinal tract. Methods: Inflammatory, preneoplastic and neoplastic conditions of the gastrointestinal tract (189 cases) were studied with the evaluation of Foxp3 regulatory T cells based on immunohistochemistry. Results: Few Foxp3(+) cells were found in controls and inflammatory conditions (oesophagitis, gastritis, coeliac disease, inflammatory bowel disease); in preneoplastic and neoplastic conditions the number of Foxp3(+) cells was significatively increased. Conclusions: In normal conditions the number of mucosal lymphocytes is very low throughout the gastro-intestinal tract; in active coeliac disease patients or on a gluten-free diet, only a slight increase in Foxp3(+) cells may be found. Gastrointestinal cancers are associated with higher Foxp3(+) cell proportion, compared with microscopically normal tissue and with precancerous conditions. However, it is uncertain whether the increase in these regulatory cells is a cause or a consequence of tumour progression. 

Retracted: No

PubPeer comments:
 Duplicated images in two papers by some of the same auuthors. Could the authors explain? ![file] , 
 Another duplication. The same image is used in different clinical settings. ![file] , 
 The authors indicate that an IRB approved the protocol but permit number is not reported. ![file] ![file] ,
YAP increases response to Trastuzumab in HER2-positive Breast Cancer by enhancing P73-induced apoptosis
Authors: Hironobu Sasano
Min Yao
Hongwen Gao
Lanqing Cao
Ping-Li Sun
Journal: Journal of Cancer (2020)
Discipline: CLINICAL MEDICINE
Keywords: Breast cancer; Chemotherapy; Neoadjuvant therapy; Protein kinase B/AKT; Tumor progression.
Affiliations: Department of Pathology, The Second Hospital of Jilin University, Changchun, Jilin 130041, China., Department of Pathology, Tohoku University School of Medicine and Tohoku University Hospital, 2-1 Seiryo-machi, Aoba-Ku, Sendai, Miyagi 980-8575, Japan.

Abstract:  The role of the Yes-associated protein (YAP) in oncogenesis and progression of breast cancer remains controversial. Meanwhile, development of therapeutic resistance to trastuzumab, a common breast cancer treatment administered after chemotherapy, is a significant challenge in the treatment of HER2-positive breast cancer. We, therefore, analyzed the role of YAP in trastuzumab resistance in HER2-positive-breast carcinoma cells in vitro and evaluated the status of YAP and related proteins in patient-derived breast carcinoma tissues by immunohistochemistry. YAP expression was observed in both BT474-TS (trastuzumab-sensitive) and BT474-TR (trastuzumab-resistant) cells. Treatment with trastuzumab increased expression of nuclear-YAP (N-YAP) in BT474-TS cells, whereas BT474-TR cells showed a decrease in N-YAP expression following trastuzumab treatment. YAP silencing significantly reduced trastuzumab-induced inhibitory effects in BT474-TS cells. YAP-silenced cells also showed decreased apoptosis and significantly lower p73 levels following trastuzumab treatment. Combined protein kinase B (AKT) inhibitor-trastuzumab treatment significantly inhibited BT474-TR cell proliferation, resulting in increased N-YAP and p73 expression, as well as apoptosis. In both paclitaxel, doxorubicin and cyclophosphamide (TAC)-treated, and docetaxel, carboplatin, and trastuzumab (TCbH)-treated groups; the pathological complete response (pCR) ratios were inversely correlated with p-AKT status in biopsy specimens, while YAP and p73 status were positively correlated with the pCR ratio in the biopsy specimens of the TCbH group. Our results show that YAP is involved in trastuzumab resistance in HER2-positive breast carcinoma cells and that YAP and AKT may be developed as prognostic markers of neoadjuvant trastuzumab therapy in patients with HER2-positive breast cancer. 

Retracted: No

PubPeer comments:
 It seems that figure 4C(YAP) is a part of figure 4G(p-AKT). ![file] , 
 #1 Thank you for your comment, we have contacted the journal and improved our figure. You can find the final version via the link below: https: www.jcancer.org v11p6748.htm ,
miR-181a down-regulates MAP2K1 to enhance adriamycin sensitivity in leukemia HL-60 cells
Authors: J-J Wang
J-P Yu
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MAPK kinase 1; MEK1; MAP2K1; microRNA-181a; leukemia
Affiliations: Department of Laboratory, Nuclear Industry 215 Hospital of Shaanxi Province, Xianyang, Shaanxi, China. .

Abstract:  Objective: MAPK kinase 1 (MEK1), also known as MAP2K1, plays a role in activating extra-cellular signal-regulated protein kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway to regulate cell proliferation and apoptosis. The abnormal expression of MAP2K1 is associated with leukemia. Bioinformatics analysis showed the targeted relationship between microRNA-181a (miR-181a) and the 3'-UTR of MAP2K1. This study aimed to investigate the role of miR-181a in regulating MAP2K1 expression, the effects on leukemic cell proliferation, apoptosis, and adriamycin (ADM) resistance. Materials and methods: Dual luciferase reporter gene assay was applied to confirm the targeted relationship between miR-181a and MAP2K1. ADM resistant cell line HL-60/ADM was established. MiR-181a and MAP2K1 expressions were detected. HL-60/ADM cells were cultured in vitro and divided into two groups, including microRNA-Normal control (miR-NC) group and miR-181a mimic group. MAP2K1, phosphorylated MAP2K1 (p-MAP2K1), and phosphorylated ERK (p-ERK) protein expressions were tested. Cell apoptosis was assessed with flow cytometry. Cell proliferation was determined using EdU staining. Results: There is a targeted regulatory relationship between miR-181a and MAP2K1 mRNA. miR-181a expression was significantly lower, while MAP2K1 mRNA and protein expressions were markedly higher in HL-60/ADM cells than HL-60 cells (p&lt;0.05). Transfection of miR-181a mimic markedly reduced expressions of MAP2K1, p-MAP2K1, and p-ERK in HL-60/ADM cells, enhanced cell apoptosis, and weakened cell proliferation compared to miR-NC (p&lt;0.05). Conclusions: MiR-181a reduction and MAP2K1 elevation were related to ADM resistance in leukemia cells. Up-regulation of miR-181a expression inhibited leukemia cell proliferation, induced apoptosis, and reduced ADM resistance via targeting MAP2K1 expression and ERK/MAPK signaling pathway. 

Retracted: Yes

PubPeer comments:
 Figure 5. Much more similar than expected. https: imgur.com 94ljYqT , 
 Figure 7A. Much more similar than expected. https: imgur.com SgEv4o4 ,
Alterations of Fas (Apo-1/CD95) gene in non-small cell lung cancer
Authors: S H Kim
S H Lee
M S Shin
W S Park
S M Dong
H S Kim
G S Park
C S Kim
N J Yoo
J Y Lee
J Y Han
J H Pi
S Y Kim
Journal: Oncogene (1999)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Fas; cell death signaling; mutations; non-lymphoid malignancies; lung cancers
Affiliations: Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul.

Abstract:  Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling. The key role of the Fas system in negative growth regulation has been studied mostly within the immune system, and somatic mutations of Fas gene in cancer patients have been described solely in lymphoid-lineage malignancies. However, many non-lymphoid tumor cells have been found to be resistant to Fas-mediated apoptosis, which suggests that Fas mutations, one of the possible mechanisms for Fas-resistance, may be involved in the pathogenesis of non-lymphoid malignancies as well. In this study, we have analysed the entire coding region and all splice sites of the Fas gene for the detection of the gene mutations in 65 human non-small cell lung cancers by polymerase chain reaction, single strand conformation polymorphism and DNA sequencing. Overall, five tumors (7.7%) were found to have the Fas mutations, which were all missense mutations. Four of the five mutations identified were located in the cytoplasmic region (death domain) known to be involved in the transduction of an apoptotic signal and one mutation was located in the transmembrane domain. This is the first report on the Fas gene mutations in non-lymphoid malignancies, and the data presented here suggests that alterations of the Fas gene might lead to the loss of its apoptotic function and contribute to the pathogenesis of some human lung cancers. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A86 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
RETRACTED: Design of curcumin-loaded PLGA nanoparticles formulation with enhanced cellular uptake, and increased bioactivity in vitro and superior bioavailability in vivo
Authors: Bokyung Sung
Preetha Anand
Rajeshwar R Tekmal
Bharat B Aggarwal
Hareesh B Nair
Vivek R Yadav
Ajaikumar B Kunnumakkara
Journal: Biochemical Pharmacology (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Curcumin; Bioavailability; Nanoparticles; PLGA; Antioxidant
Affiliations: Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX 77030, USA.

Abstract:  Curcumin, a yellow pigment present in the spice turmeric (Curcuma longa), has been linked with antioxidant, anti-inflammatory, antiproliferative, anticancer, antidiabetic, antirheumatic, and antiviral effects, but its optimum potential is limited by its lack of solubility in aqueous solvents and poor oral bioavailability. We employed a polymer-based nanoparticle approach to improve bioavailability. Curcumin was encapsulated with 97.5% efficiency in biodegradable nanoparticulate formulation based on poly (lactide-co-glycolide) (PLGA) and a stabilizer polyethylene glycol (PEG)-5000. Dynamic laser light scattering and transmission electron microscopy indicated a particle diameter of 80.9 nm. This curcumin, renamed from hereon "as curcumin (NP)", was characterized for its biological activity. In vitro curcumin (NP) exhibited very rapid and more efficient cellular uptake than curcumin. Estrase staining revealed that curcumin (NP) was at least as potent as or more potent than curcumin in inducing apoptosis of leukemic cells and in suppressing proliferation of various tumor cell lines. When examined by electrophoretic gel shift mobility assay, curcumin (NP) was more active than curcumin in inhibiting TNF-induced NF-kappaB activation and in suppression of NF-kappaB-regulated proteins involved in cell proliferation (cyclin D1), invasion (MMP-9), and angiogenesis (VEGF). In mice, curcumin (NP) was more bioavailable and had a longer half-life than curcumin. Overall we demonstrate that curcumin-loaded PLGA nanoparticles formulation has enhanced cellular uptake, and increased bioactivity in vitro and superior bioavailability in vivo over curcumin. 

Retracted: Yes

PubPeer comments:
null, 
null, 
 Here is an illustration of the image panel similarities described in the retraction notice, marked with boxes of the same color. ![file] , 
 Not mentioned in the retraction notice of this article is the similarity between lanes in Figure 4 that represent different conditions, shown here with red boxes. A very similar issue was noted for Yadav et al., DOI: 10.1016 j.bcp.2010.06.022 as shown here: https: pubpeer.com publications 7460E0738A16FAE33340D97491CE5C ![file] ,
MicroRNA 483-3p targets Pard3 to potentiate TGF-β1-induced cell migration, invasion, and epithelial–mesenchymal transition in anaplastic thyroid cancer cells
Authors: Zhongwei Lv
Lin Liu
Xianzhao Deng
Haidong Cai
Bo Wu
Youben Fan
Yushui Ma
Dan Li
Chengyou Jia
Xiaoping Zhang
Journal: Oncogene (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Anaplastic thyroid cancer; MicroRNA 483-3p; Pard3; tumorigenesis; cell polarity
Affiliations: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China., Shanghai Center of Thyroid Diseases, Shanghai, 200072, China., Center of Thyroid, Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China., Center of Thyroid, Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. ., Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. ., Shanghai Center of Thyroid Diseases, Shanghai, 200072, China. .

Abstract:  Anaplastic thyroid cancer (ATC) is associated with poor prognosis and is often untreatable. MicroRNA 483-3p (miR-483) and partitioning-defective 3 (Pard3), a member of the Pard family, have functions and regulatory mechanisms in ATC. The abnormal regulation of miR-483 may play an important role in tumorigenesis, and Par3 is known to regulate cell polarity, cell migration, and cell division. Tumor proliferation promoted by the regulation of miRNA expression can be regulated in thyroid cancer by upregulating transforming growth factor-β1 (TGF-β1), which is thought to interact with Pard3. When compared with adjacent non-tumor tissues, we found that miR-483 was upregulated and Pard3 was downregulated in 80 thyroid tumor samples. Disease-free survival was decreased when expression of miR-483 was upregulated and Pard3 expression was downregulated. Cell growth, migration, and invasion were induced by overexpression of miR-483. However, knockdown of miR-483 resulted in a loss of cell invasion and viability, both in vitro and in vivo. The expression of Pard3 was increased by the inhibition of miR-483, but TGF-β1-induced cell migration and invasion were decreased by miR-483 inhibition. A dual-luciferase reporter assay determined that Pard3 expression was downregulated when targeted with miR-483. The epithelial-mesenchymal transition (EMT), as well as Tiam1-Rac signaling, was induced by TGF-β1, which was decreased by the overexpression of Pard3. Pard3 decreased the inhibition of EMT and Tiam-Rac1 signaling, which resulted from transfection of ATC cells with miR-483. Overall, the results showed that downregulation of Pard3 resulted in increased cell invasion and EMT in ATC, which was promoted by treatment with miR-483. These findings suggest novel therapeutic targets and treatment strategies for this disease. 

Retracted: No

PubPeer comments:
 Image appears duplicated ![file] , 
 Image may be smeared ![file] ,
Tripartite Motif-containing 33 (TRIM33) protein functions in the poly(ADP-ribose) polymerase (PARP)-dependent DNA damage response through interaction with Amplified in Liver Cancer 1 (ALC1) protein
Authors: Simon J Boulton
Antoinette R Tan
Antonia Tomas-Loba
Zuzana Horejsi
Ming Yao
Shridar Ganesan
Atul Kulkarni
Jay Oza
Vasudeva Ginjala
Honeah Sohail
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ALC1; ATPases; Cancer Biology; Cell Signaling; Chromatin
Affiliations: From the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903., the DNA Damage Response Laboratory, London Research Institute, Clare Hall, South Mimms, EN6 3LD Herts, United Kingdom., From the Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey 08903. Electronic address: .

Abstract:  Activation of poly(ADP-ribose) polymerase (PARP) near sites of DNA breaks facilitates recruitment of DNA repair proteins and promotes chromatin relaxation in part through the action of chromatin-remodeling enzyme Amplified in Liver Cancer 1 (ALC1). Through proteomic analysis we find that ALC1 interacts after DNA damage with Tripartite Motif-containing 33 (TRIM33), a multifunctional protein implicated in transcriptional regulation, TGF-β signaling, and tumorigenesis. We demonstrate that TRIM33 is dynamically recruited to DNA damage sites in a PARP1- and ALC1-dependent manner. TRIM33-deficient cells show enhanced sensitivity to DNA damage and prolonged retention of ALC1 at sites of DNA breaks. Conversely, overexpression of TRIM33 alleviates the DNA repair defects conferred by ALC1 overexpression. Thus, TRIM33 plays a role in PARP-dependent DNA damage response and regulates ALC1 activity by promoting its timely removal from sites of DNA damage. 

Retracted: No

PubPeer comments:
 Figure 1B. Much more similar than expected. ![file] ,
Enhanced Anti-Cancer Effect of Snake Venom Activated NK Cells on Lung Cancer Cells by Inactivation of NF-κB
Authors: Do Hee Won
Pushpa Saranya Kollipara
Min Jong Song
Yu Yeon Jung
Jin Tae Hong
Chul Ju Hwang
Mi Hee Park
Heui Seoung Yoon
Ho Sueb Song
Journal: Biomolecules & Therapeutics (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Death receptor; Lung cancer; NF-κB; NK-92MI cells; Snake venom.
Affiliations: College of Pharmacy and Medical Research Center, Chungbuk National University, Cheongju 361-763, Republic of Korea, Department of Obstetrics and Gynecology, Daejeon St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Republic of Korea, College of Korean Medicine, Gachon University, Seongnam 461-701, Republic of Korea

Abstract:  In the present study, we investigated anti-cancer effect of snake venom activated NK cells (NK-92MI) in lung cancer cell lines. We used snake venom (4 μg/ml) treated NK-92MI cells to co-culture with lung cancer cells. There was a further decrease in cancer cell growth up to 65% and 70% in A549 and NCI-H460 cell lines respectively, whereas 30-40% was decreased in cancer cell growth by snake venom or NK-92MI alone treatment. We further found that the expression of various apoptotic proteins such as that Bax, and cleaved caspase-3 as well as the expression of various death receptor proteins like DR3, DR4 and Fas was also further increased. Moreover, consistent with cancer cell growth inhibition, the DNA binding activity of NF-κB was also further inhibited after treatment of snake venom activated NK-92MI cells. Thus, the present data showed that activated NK cells could further inhibit lung cancer cell growth. 

Retracted: No

PubPeer comments:
 Figure 1 appears to have a repeated image. *** ![file] ,
Cytoprotective effects of cerium and selenium nanoparticles on heat-shocked human dermal fibroblasts: an in vitro evaluation
Authors: Amit K Roy
Bo Yuan
Thomas J Webster
Journal: International Journal of Nanomedicine (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: cell death; ceria; heat shock; nanomedicine; nanotechnology
Affiliations: Chemical Engineering Department, College of Engineering, Northeastern University, Boston, MA, USA.

Abstract:  It is a widely accepted fact that environmental factors affect cells by modulating the components of subcellular compartments and altering metabolic enzymes. Factors (such as oxidative stress and heat-shock-induced proteins and heat shock factors, which upregulate stress-response related genes to protect affected cells) are commonly altered during changes in environmental conditions. Studies by our group and others have shown that nanoparticles (NPs) are able to efficiently attenuate oxidative stress by penetrating into specific tissues or organs. Such findings warrant further investigation on the effects of NPs on heat-shock-induced stress, specifically in cells in the presence or absence (pretreated) of NPs. Here, we examined the cytoprotective effects of two different NPs (cerium and selenium) on heat-induced cell death for a model cell using dermal fibroblasts. We report for the first time that both ceria and selenium NPs (at 500 µg/mL) possess stress-relieving behavior on fibroblasts undergoing heat shock. Such results indicate the need to further develop these NPs as a novel treatment for heat shock. 

Retracted: No

PubPeer comments:
 Could the authors examine the images in figures for five and six? It isnu2019t clear that these images marked (in various colors) should appear so similar, given the description of the conditions. *** ![file] , 
 We are looking into this. , 
 These figures have been verified as published in the manuscript - Tom Webster , 
 #3 This is a confusing response. Is the author suggesting that these images are not repeated? Selecting one example and showing below in higher resolution, the images outlined in magenta appear to the eye as exact duplicates. Also confirmed using Forensically. Could the authors take a second look? *** ![file] *** Forensically ![file] , 
 We apologize as we were looking at the wrong paper since the authors listed above are incorrect for this paper and the figures in question. We are looking further into this. , 
 Any update on this? , 
 Corrigendum Accepted for publication 31 May 2021 The authors inadvertently duplicated several images across Figures 4, 5 and 6 on pages 1431 and 1432 in the original publication. Figure 4 Ce (500 u00b5g mL) 37u00b0C 24 h was duplicated with Figure 5 Ce (500 u00b5g mL) 37u00b0C 48 h; Figure 5 Control 37u00b0C 48 h was duplicated with Figure 5 Se 37u00b0C 48 h and Figure 4 Se (500 u00b5g mL) 42u00b0C 24 h was duplicated with Figure 6 Se 42u00b0C 72 h. The correct Figures 4, 5 and 6 are shown below. The authors have advised that this does not change the conclusion of the paper. ![file] ![file] ![file] ,