PReD-Bench/PRed-Bench huggingface dataset:
A modified method by differential adhesion and serum-free culture medium for enrichment of cancer stem cells
Authors: Cheng-Yong Lei
Chun-Yan Wang
Wan-Long Tan
Yong-Tong Zhu
Yang Luo
Shi-Yu Pang
Journal: Journal of cancer research and therapeutics (2018)
Discipline: CLINICAL MEDICINE
Keywords: Cancer stem cells; resistant; sensitive; serum-free culture; trypsin.
Affiliations: Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Nanfang Hospital; Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, China., Department of Neurology, TCM-Integrated Cancer Center of Southern Medical University, Guangzhou, China., Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Abstract:  Objective: In this study, we showed a modified method for the isolation of cancer stem cells (CSCs) using a combination of differential adhesion method and serum-free culture medium (SFM) method. Materials and methods: Trypsin-sensitive cells and trypsin-resistant cells were isolated from MB49, EJ, and SK-OV-3 cells using a combination of differential adhesion method and SFM method. The CSCs markers expression of trypsin-resistant cells was verified by the flow cytometry, the Western blotting, and the quantitative polymerase chain reaction. Functional comparisons were verified by the resistance to chemotherapy assay, the transwell assay, and the tumor xenograft formation assay. Results: Trypsin-resistant cells were isolated successfully. They were identified with high expression of CSCs markers and possessed higher resistance to chemotherapy, greater migration in vitro and stronger tumorigenic abilities in vivo. Conclusion: Trypsin-resistant cells showed specific CSCs characterizations. They were able to be isolated successfully with a modified method by a combination of differential adhesion method and SFM method. 

Retracted: No

PubPeer comments:
 Xenograft mice in the Fig.4B were already published before as completely different experiments: doi:10.1590 S1677-5538.IBJU.2015.0409 - Fig.3B, doi:10.1186 s13287-015-0211-1 - Fig.1F, doi:10.1016 j.scr.2014.04.006 - Fig.4E, doi:10.1186 1471-2490-13-57 - Fig.4E. # **Fig.4B**  # **Fig.3B (doi:10.1590 S1677-5538.IBJU.2015.0409)**  # **Fig.1F (doi:10.1186 s13287-015-0211-1)**  # **Fig.4E (doi:10.1016 j.scr.2014.04.006)**  # **Fig.4E (doi:10.1186 1471-2490-13-57)**  , 
 Figure 3. Two of the flow cytometry panels look more similar than expected. Boxes of the same color show areas that look very similar.  ,
Prion diseases of humans and farm animals: epidemiology, genetics, and pathogenesis
Authors: Adriano Aguzzi
Journal: Journal of Neurochemistry (2006)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Neuronal vacuolation; spongiosis; neuronal death; glial reactions; transmissible spongiform encephalopathies
Affiliations: Institute of Neuropathology, Universit√§tsspital Z√ºrich, Z√ºrich, Switzerland. 

Abstract:  Neuronal vacuolation (spongiosis), neuronal death, and pronounced glial reactions are the hallmarks of transmissible spongiform encephalopathies (TSEs), or prion diseases. A wealth of physical, biochemical, and immunological evidence indicates that the TSE agent, termed prion, does not contain agent-specific nucleic acid encoding its own constituents, as is the case for all other infectious pathogens. Also, no adaptive immune responses are elicited upon infection. A defining feature of TSEs is the deposition, mainly in the brain and lymphoreticular tissues, of an aggregated and structurally abnormal protein, designated PrP(Sc) or PrP-res, which represents a conformational isomer of the ubiquitous surface protein PrP(C). Biochemical and genetic evidence link PrP and its gene to the disease. Although TSEs are by definition transmissible, a growing number of Prnp-associated non-infectious neurodegenerative proteinopathies are now being recognized. 

Retracted: No

PubPeer comments:
 No - the ACE2 receptor is not a gene. ,
Interaction of RAS activation and lipid disorders accelerates the progression of glomerulosclerosis
Authors: Yu Wu
Kun-Ling Ma
Jie Ni
Bi-Cheng Liu
Yang Zhang
Chang-Xian Wang
Xiong-Zhong Ruan
Jing Liu
Lin-Li Lv
Journal: International Journal of Medical Sciences (2013)
Discipline: CLINICAL MEDICINE
Keywords: extracellular matrix; glomerulosclerosis; lipid disorder; low-density lipoprotein receptor; renin-angiotensin system.
Affiliations: 1. Institute of Nephrology, Zhong Da Hospital, Southeast University School of Medicine, Nanjing City, Jiangsu Province, P.R. China.

Abstract:  Background: The activation of the renin-angiotensin system (RAS) and lipid disorders are major risk factors in progressive chronic kidney disease. This study aimed to investigate the potential synergistic mechanisms of RAS activation and lipid disorders that contribute to glomerulosclerosis. Materials and methods: Human renal mesangial cells (HMCs) were treated with 10(-7) mol/L angiotensin II (Ang II) or with 30 Œºg/ml cholesterol and 1 Œºg/ml 25-hydroxycholesterol (lipid loading) for 24 hours. Lipid accumulation in the cells was evaluated by Oil Red O staining and intracellular cholesterol quantitative assays. The gene and protein expression of molecules in the low-density lipoprotein receptor (LDLr) pathway, the RAS family, and the extracellular matrix were examined by real-time polymerase chain reaction and Western blotting. The translocation of sterol regulatory element-binding protein (SREBP) cleavage activating protein (SCAP), which escorts SREBP-2 from the endoplasmic reticulum (ER) to the Golgi, was examined by immunofluorescent staining. Results: Ang II increased lipid droplet accumulation in HMCs. Further analysis revealed that Ang II increased the mRNA and protein expression of LDLr, SCAP, and SREBP-2. This increase was correlated with an enhanced translocation of the SCAP/SREBP-2 complex from the ER to the Golgi in HMCs that was induced by Ang II, thereby activating LDLr gene transcription. Interestingly, lipid loading increased the mRNA and protein expression of angiotensinogen, Ang II, renin, angiotensin-converting enzyme, angiotensin II type 1 receptor, and type 2 receptor in HMCs with increased mRNA and protein expression of collagen I, Œ±-smooth muscle actin, and fibronectin. Conclusions: This study demonstrates that the interaction of RAS activation and lipid disorders accelerates the progression of glomerulosclerosis. 

Retracted: No

PubPeer comments:
 image duplications  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. ,
<p>ZFAS1 Promotes Cisplatin Resistance via Suppressing miR-421 Expression in Oral Squamous Cell Carcinoma</p>
Authors: Fengjuan Wang
Rui Hao
Fan Wang
Xiaolong Wang
Journal: Cancer Management and Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: ZFAS1; chemoresistance; cisplatin; exosome; miR-421
Affiliations: Department of Stomatology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, People's Repubic of China., Department of Oncology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, People's Repubic of China.

Abstract:  Purpose: Oral squamous cell carcinoma (OSCC), with high incidence and mortality, represents one of the main reasons for head and neck malignant tumors. We want to investigate the effect of ZFAS1 on DDP resistance in oral squamous cell carcinoma. Methods: The proliferation and migration of cells was detected by CCK-8 and Transwell assay. The apoptosis was measured by flow cytometry and Western blot. The interaction of ZFAS1, miR-421, and MEIS2 was verified by luciferase reporter assay. The role of ZFAS1 in DDP resistance in vivo was tested by the nude mice model. The expression of ZFAS1 in exosomes from cisplatin-resistant patients was also determined. Results: ZFAS1 overexpression improved OSCC cell growth and inhibited OSCC cell susceptibility to DDP. In addition, the silencing of ZFAS1 promoted DDP-induced apoptosis. ZFAS1 directly bound to miR-421, which was verified by luciferase reporter assay. Inhibition of miR-421 reversed the effect of si-ZFAS1, which promoted the cell viability and decreased the sensitivity of DDP in DDP-resistant cells. The in vivo experiment showed the role of ZFAS1 in increasing the DDP resistance in OSCC tumor. Importantly, this study also showed upregulated ZFAS1 in serum exosomes derived from cisplatin-resistant patients. Conclusion: ZFAS1 promotes chemoresistance of oral squamous cell carcinoma to cisplatin and might become a latent therapeutic target for treating OSCC. 

Retracted: No

PubPeer comments:
 Figure 3K. After stretching, the two group of u03b2-actin look the same.  ,
Identification of tRNA-derived small RNA (tsRNA) responsive to the tumor suppressor, RUNX1, in breast cancer
Authors: Nicholas H Farina
Andrew J Fritz
Veronica Balatti
Janet L Stein
Deli Hong
Jane B Lian
Gary S Stein
Dario Veneziano
Carlo M Croce
Caroline E Adams
Stephanie Scalia
Terri L Messier
Journal: Journal of cellular physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RUNX1; breast cancer; ncRNA; tRNA-derived fragments (tRF); tRNA-derived small RNA (tsRNA).
Affiliations: Department of Biochemistry, Larner College of Medicine, University of Vermont, Burlington, Vermont., Larner College of Medicine, University of Vermont Cancer Center, Burlington, Vermont., Northern New England Clinical and Translational Research Network., Department of Pharmacology, Larner College of Medicine, University of Vermont, Burlington, Vermont., Department of Cancer Biology and Medical Genetics, The Ohio State University Comprehensive Cancer Center, Columbus, Ohio., Department of Surgery, Larner College of Medicine, University of Vermont, Burlington, Vermont.

Abstract:  Despite recent advances in targeted therapies, the molecular mechanisms driving breast cancer initiation, progression, and metastasis are minimally understood. Growing evidence indicate that transfer RNA (tRNA)-derived small RNAs (tsRNA) contribute to biological control and aberrations associated with cancer development and progression. The runt-related transcription factor 1 (RUNX1) transcription factor is a tumor suppressor in the mammary epithelium whereas RUNX1 downregulation is functionally associated with breast cancer initiation and progression. We identified four tsRNA (ts-19, ts-29, ts-46, and ts-112) that are selectively responsive to expression of the RUNX1 tumor suppressor. Our finding that ts-112 and RUNX1 anticorrelate in normal-like mammary epithelial and breast cancer lines is consistent with tumor-related activity of ts-112 and tumor suppressor activity of RUNX1. Inhibition of ts-112 in MCF10CA1a aggressive breast cancer cells significantly reduced proliferation. Ectopic expression of a ts-112 mimic in normal-like mammary epithelial MCF10A cells significantly increased proliferation. These findings support an oncogenic potential for ts-112. Moreover, RUNX1 may repress ts-112 to prevent overactive proliferation in breast epithelial cells to augment its established roles in maintaining the mammary epithelium. 

Retracted: No

PubPeer comments:
 The values shown in Figure 2b-e show extremely low variation. Isn t it surprising to get so similar clustering of values, as shown here?  ,
Targeting the AIB1 oncogene through mammalian target of rapamycin inhibition in the mammary gland
Authors: Andrew L Kung
Myles Brown
Jing Yuan
Maria I Torres-Arzayus
Heidi Lane
Jamie L DellaGatta
Journal: Cancer Research (2006)
Discipline: CLINICAL MEDICINE
Keywords: AIB1; estrogen receptor; breast cancer; transgenic mouse model; premalignant phenotype
Affiliations: Division of Molecular and Cellular Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.

Abstract:  Amplified in breast cancer 1 (AIB1), an estrogen receptor (ER) coactivator, is frequently amplified or overexpressed in human breast cancer. We previously developed a transgenic mouse model in which AIB1 can act as an oncogene, giving rise to a premalignant hyperplastic mammary phenotype as well as to a high incidence of mammary tumors that are primarily ER(+). In this model, the AIB1 transgene is responsible for continued activation of the insulin-like growth factor-I receptor, suggesting a role for the activation of the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (mTOR) pathway in the premalignant phenotype and tumor development. Here we show that treatment of AIB1 transgenic mice with the mTOR inhibitor RAD001 reverts the premalignant phenotype. Furthermore, treatment of cell lines derived from AIB1-dependent mammary tumors with RAD001 in culture leads to a G(1) cell cycle arrest. Lastly, tumor growth after injection of ER(+) AIB1 tumor cell lines into wild-type animals is inhibited by RAD001 treatment. In this ER(+) model, inhibition of tumor growth by RAD001 was significantly better than inhibition by the antiestrogen 4-hydroxytamoxifen alone, whereas a combination of both RAD001 and 4-hydroxytamoxifen was most effective. Based on these results, we propose that the combination of mTOR inhibition and ER-targeted endocrine therapy may improve the outcome of the subset of ER(+) breast cancers overexpressing AIB1. These studies provide preclinical support for the clinical development of RAD001 and suggest that AIB1 may be a predictive factor of RAD001 response. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than expected.  ,
Upregulation of SNHG6 regulates ZEB1 expression by competitively binding miR-101-3p and interacting with UPF1 in hepatocellular carcinoma
Authors: Zhisu Liu
Lei Chang
Cuicui Li
Yufeng Yuan
Haolong Qi
Xu Dong
Tao Guo
Yusha Xiao
Quanyan Liu
Journal: Cancer Letters (2016)
Discipline: CLINICAL MEDICINE
Keywords: EMT; Hepatocellular carcinoma; UPF1; ZEB1; snoRNA host gene 6 (SNHG6).
Affiliations: Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, PR China., Zhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan, 430071, PR China., Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical College, Haikou, Hainan, 571199, PR China., Department of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, PR China. Electronic address: .

Abstract:  Emerging evidence suggests that small nucleolar RNAs (snoRNAs) and their host genes (SNHGs) have malfunctioning roles in the development of human cancers. We globally investigated the molecular mechanisms by which snoRNA host gene 6 (SNHG6) promotes hepatocellular carcinoma (HCC) progression using human tissues and cell lines. We found that SNHG6 is overexpressed in HCC tissues and in hepatoma cell lines and is closely associated with histologic grade, hepatitis B virus DNA, Barcelona Clinic Liver Cancer stage and portal vein tumor thrombus in patients with HCC. Knockdown of SNHG6 induced apoptosis and repressed cell cycle progression in hepatoma cell lines, whereas transgenic expression of SNHG6 in the immortalized human hepatic cell line L02 had opposite effects. Xenograft tumors grown from SNHG6-knockdown cells had smaller mean volumes than did tumors grown from control cells. SNHG6 may act as a competing endogenous RNA, effectively becoming a sink for miR-101-3p and thereby modulating the derepression of zinc finger E-box binding homeobox 1, imposing an additional level of post-transcriptional regulation. Functionally, SNHG6 promotes tumor growth and metastasis by inducing epithelial to mesenchymal transition. Further investigations showed that SNHG6 could affect HCC tumorigenesis by binding to up-frameshift protein 1 and regulating Smad7 expression. 

Retracted: No

PubPeer comments:
 Fig 3D.  SNHG6 knockdown represses hepatoma cell proliferation, invasion and migration in vitro. ... (D) Cell invasion assays performed using HCCLM9 cells or Huh7 cells after SNHG6 knockdown . I have concerns.  ,
Sirtuin 3 promotes microglia migration by upregulating CX3CR1
Authors: Junxiang Yin
Jiong Shi
Shiping Li
Li Guo
Runjing Cao
Journal: Cell Adhesion & Migration (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CX3CR1; Ischemia; SIRT3; microglia migration.
Affiliations: a Department of Neurology , The Second Hospital of Hebei Medical University , Shijiazhuang , China., b Barrow Neurological Institute , St. Joseph Hospital and Medical Center, Dignity Health Organization , Phoenix , AZ , USA., c Advanced Innovation Center for Human Brain Protection , Capital Medical University , Beijing , China., d China National Clinical Research Center for Neurological Diseases, Department of Neurology , Beijing Tiantan Hospital, Capital Medical University , Beijing , China.

Abstract:  We studied the role of Sirtuin 3 (SIRT3) in microglial cell migration in ischemic stroke. We used a middle cerebral artery occlusion (MCAO) model of focal ischemia. We then applied lentivirus-packaged SIRT3 overexpression and knock down in microglial N9 cells to investigate the underlying mechanism driving microglial cell migration. More microglial cells appeared in the ischemic lesion side after MCAO. The levels of SIRT3 were increased in macrophages, the main source of microglia, after ischemia. CX3CR1 levels were increased with SIRT3 overexpression. SIRT3 promoted microglial N9 cells migration by upregulating CX3CR1 in both normal and glucose deprived culture media. These effects were G protein-dependent. Our study for the first time shows that SIRT3 promotes microglia migration by upregulating CX3CR1. 

Retracted: No

PubPeer comments:
 Same image different treatments. Could the author please check?  ,
Disease-relevant proteostasis regulation of cystic fibrosis transmembrane conductance regulator
Authors: M Pettoello-Mantovani
E M Bruscia
A Luini
M Vicinanza
M C Maiuri
V Raia
R Carnuccio
S Cenci
V R Villella
M A De Matteis
L Maiuri
S Guido
S Esposito
G Kroemer
Journal: Cell death and differentiation (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Protein trafficking; Proteostasis network; Cystic fibrosis; CFTR; Rab5
Affiliations: Division of Genetics and Cell Biology, San Raffaele Scientific Institute, European Institute for Research in Cystic Fibrosis, Milan 20132, Italy.

Abstract:  Mismanaged protein trafficking by the proteostasis network contributes to several conformational diseases, including cystic fibrosis, the most frequent lethal inherited disease in Caucasians. Proteostasis regulators, as cystamine, enable the beneficial action of cystic fibrosis transmembrane conductance regulator (CFTR) potentiators in ŒîF508-CFTR airways beyond drug washout. Here we tested the hypothesis that functional CFTR protein can sustain its own plasma membrane (PM) stability. Depletion or inhibition of wild-type CFTR present in bronchial epithelial cells reduced the availability of the small GTPase Rab5 by causing Rab5 sequestration within the detergent-insoluble protein fraction together with its accumulation in aggresomes. CFTR depletion decreased the recruitment of the Rab5 effector early endosome antigen 1 to endosomes, thus reducing the local generation of phosphatidylinositol-3-phosphate. This diverts recycling of surface proteins, including transferrin receptor and CFTR itself. Inhibiting CFTR function also resulted in its ubiquitination and interaction with SQSTM1/p62 at the PM, favoring its disposal. Addition of cystamine prevented the recycling defect of CFTR by enhancing BECN1 expression and reducing SQSTM1 accumulation. Our results unravel an unexpected link between CFTR protein and function, the latter regulating the levels of CFTR surface expression in a positive feed-forward loop, and highlight CFTR as a pivot of proteostasis in bronchial epithelial cells. 

Retracted: No

PubPeer comments:
 Fig. 7A: More similar than expected. Could authors check it please?  Zoom:  ,
In vivo and in vitro protective effects of omeprazole against neuropathic pain
Authors: Chandragouda R Patil
Sanjay K Chanchal
Sumit Siddharth
Sameer N Goyal
Umesh B Mahajan
Chanakya N Kundu
Navyya Reddy
Basavaraj P Bommanahalli
Shreesh Ojha
Prakash H Patil
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: omeprazole; neuropathic pain; inflammatory cytokines; neuroprotective effect; oxidative stress
Affiliations: Department of Pharmacology, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Dist-Dhule-425405, Maharashtra, India., Department of Pathology, Gadag Institute of Medical Sciences, Bommanahalli, Gadag-582101, Karnataka, India., Cancer Biology Laboratory, KIIT School of Biotechnology, KIIT University, Bhubaneswar-721024, Odisha, India., Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi 17666, United Arab Emirates.

Abstract:  Apart from reducing the acid secretion, omeprazole inhibits activation of the nuclear factor-Œ∫B, release of inflammatory cytokines, and chemotaxis of neutrophils. These mechanisms prompted us to evaluate antineuropathic effect of omeprazole in the chronic constriction injury (CCI)-induced rat model of neuropathic pain and LPS mediated ROS-induced U-87 cells. Omeprazole at 50 mg/kg/day/oral for 14 days significantly reduced the intensity of neuropathic pain estimated as paw withdrawal latency, withdrawal pressure threshold and restored the motor nerve conduction velocity in the constricted nerve, when compared with respective groups. The histological findings revealed the protective effect of omeprazole against the CCI-induced damage. Omeprazole significantly decreased the levels of tumor necrosis factor (TNF-Œ±), interleukin-1Œ≤ (IL-1Œ≤) and interleukin-6 (IL-6) as compared to their respective control groups. It also reduced the oxidative stress by up regulating the SOD, catalase activity and decreasing MDA content. Similarly, in-vitro study, LPS mediated ROS-induced U-87 cells, omeprazole reduced the oxidative stress as well as the release of TNF-Œ±, IL-1Œ≤ and IL-6. Altogether, these results suggest that, neuroprotective effect of omeprazole is mediated through preventing release of proinflammatory cytokines, augmenting endogenous anti-oxidant defense system, and maintain the structural integrity of sciatic nerve from the CCI-induced structural damage and inflammatory changes. 

Retracted: No

PubPeer comments:
 This paper is mentioned in a Retraction Watch article. http: retractionwatch.com 2019 06 11 permeable-to-bad-science-journal-retracts-paper-hailed-by-proponents-of-homeopathy #more-100085 u201cBucci flagged two other other papers by Patil, one in the journal Homeopathy, and one also in Scientific Reports. A spokesperson for the latter journal told Retraction Watch: Our investigation into this paper is still ongoing. Once this has been completed, we will take action where appropriate.u201d ,
NPM-ALK oncogenic kinase promotes cell-cycle progression through activation of JNK/cJun signaling in anaplastic large-cell lymphoma
Authors: L Jeffrey Medeiros
Megan S Lim
George Z Rassidakis
Francois X Claret
Elias Drakos
Kojo S Elenitoba-Johnson
Vasiliki Leventaki
Journal: Blood (2007)
Discipline: CLINICAL MEDICINE
Keywords: Anaplastic large-cell lymphoma; NPM-ALK; JNK; cJun; AP-1
Affiliations: Department of Hematopathology,, Department of Pathology, University of Michigan, Ann Arbor, Department of Molecular Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston;

Abstract:  Anaplastic large-cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35), resulting in aberrant expression of nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). We show that in 293T and Jurkat cells, forced expression of active NPM-ALK, but not kinase-dead mutant NPM-ALK (210K&gt;R), induced JNK and cJun phosphorylation, and this was linked to a dramatic increase in AP-1 transcriptional activity. Conversely, inhibition of ALK activity in NPM-ALK(+) ALCL cells resulted in a concentration-dependent dephosphorylation of JNK and cJun and decreased AP-1 DNA-binding. In addition, JNK physically binds NPM-ALK and is highly activated in cultured and primary NPM-ALK(+) ALCL cells. cJun phosphorylation in NPM-ALK(+) ALCL cells is mediated by JNKs, as shown by selective knocking down of JNK1 and JNK2 genes using siRNA. Inhibition of JNK activity using SP600125 decreased cJun phosphorylation and AP-1 transcriptional activity and this was associated with decreased cell proliferation and G2/M cell-cycle arrest in a dose-dependent manner. Silencing of the cJun gene by siRNA led to a decreased S-phase cell-cycle fraction associated with upregulation of p21 and downregulation of cyclin D3 and cyclin A. Taken together, these findings reveal a novel function of NPM-ALK, phosphorylation and activation of JNK and cJun, which may contribute to uncontrolled cell-cycle progression and oncogenesis. 

Retracted: No

PubPeer comments:
 Figure 4F. Much more similar than you would expect. https: imgur.com U3Nm8Ls , 
 #1 I agree. Background noise also appears the same. *** Inverse, contrast enhanced  *** False color, enhanced contrast  ,
The effect of curcumin on cell adhesion of human esophageal cancer cell
Authors: T-D Liu
X Kang
G Chen
J-X Zhang
B-Z Zheng
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Esophageal cancer; Curcumin; Cell adhesion; Apoptosis; Reactive oxygen species
Affiliations: Department of Radiotherapy, Shanxi Province Tumor Hospital, Taiyuan, Shan Xi, China. .

Abstract:  Objective: Esophageal cancer is the 8th most common cancers worldwide and the 6th most common cause of death among cancers. Curcumin has been reported to have the function of anti-inflammatory, antioxidant, anti-rheumatoid, and anti-atherosclerosis role. It can also reduce lipid, eliminate free radicals and inhibit the growth of the tumor. Many reports had suggested that curcumin has shown great potential in the treatment of tumors by inducing apoptosis. Little is known about the effects of curcumin on cell adhesion of tumor cancer. Therefore, in this study, we attempted to look for a new approach to target resistant cells and improve efficacy without toxicity. Materials and methods: Human esophageal cancer cell line (Eca-109 cells) was cultured. Cell adhesion was detected under a microplate reader. Reactive oxygen species were measured using Fluostar Omega Spectrofluorimeter. SOD activity and GSH content in cells were detected by commercial determination kit. The expression of p-JAK, p-STAT3 and STAT3 were measured by Western blot and RT-PCR. Results: Cell adhesion assay showed curcumin enhances cell-cell adhesion and cell-matrix adhesion in Eca-109 cells. ROS levels, SOD activity and total GSH content were detected and the results showed curcumin decreases intracellular ROS levels but increases SOD activity and total GSH content. Then, NAC (ROS inhibitor) and ICI (ER inhibitor) were pre-treated. Results showed ICI reversed the decreasing of intracellular ROS levels and the increasing of SOD activity and total GSH content affected by curcumin, but NAC had no such impact. Taken together, ER rather than ROS involves in cell adhesion affected by curcumin. Meanwhile, the downregulating of p-JAK, p-SATA3 and total STAT3 were caused by curcumin but NAC had no such influence. They were reversed by ICI, but NAC had no such influence. Conclusions: Curcumin could increase cell adhesion through inhibiting JAK/STAT3 mediated by ER in Eca-109. 

Retracted: No

PubPeer comments:
 Figure 4A. * Red boxes: Two panels appear to show an overlap.  ,
Minocycline suppresses interleukine-6, its receptor system and signaling pathways and impairs migration, invasion and adhesion capacity of ovarian cancer cells: in vitro and in vivo studies
Authors: Parvin Ataie-Kachoie
David L Morris
Mohammad H Pourgholami
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: IL-6; ovarian cancer; minocycline; signaling pathways; STAT3
Affiliations: Department of Surgery, University of New South Wales, St George Hospital, Sydney, New South Wales, Australia.

Abstract:  Interleukin (IL)-6 has been shown to be a major contributing factor in growth and progression of ovarian cancer. The cytokine exerts pro-tumorigenic activity through activation of several signaling pathways in particular signal transducer and activator of transcription (STAT3) and extracellular signal-regulated kinase (ERK)1/2. Hence, targeting IL-6 is becoming increasingly attractive as a treatment option in ovarian cancer. Here, we investigated the effects of minocycline on IL-6 and its signaling pathways in ovarian cancer. In vitro, minocycline was found to significantly suppress both constitutive and IL-1Œ≤ or 4-hydroxyestradiol (4-OH-E2)-stimulated IL-6 expression in human ovarian cancer cells; OVCAR-3, SKOV-3 and CAOV-3. Moreover, minocycline down-regulated two major components of IL-6 receptor system (IL-6RŒ± and gp130) and blocked the activation of STAT3 and ERK1/2 pathways leading to suppression of the downstream product MCL-1. In female nude mice bearing intraperitoneal OVCAR-3 tumors, acute administration (4 and 24 h) of minocycline (30 mg/kg) led to suppression of IL-6. Even single dose of minocycline was effective at significantly lowering plasma and tumor IL-6 levels. In line with this, tumoral expression of p-STAT3, p-ERK1/2 and MCL-1 were decreased in minocycline-treated mice. Evaluation of the functional implication of minocycline on metastatic activity revealed the capacity of minocycline to inhibit cellular migration, invasion and adhesion associated with down-regulation of matrix metalloproteinases (MMP)-2 and 9. Thus, the data suggest a potential role for minocycline in suppressing IL-6 expression and activity. These effects may prove to be an important attribute to the upcoming clinical trials of minocycline in ovarian cancer. 

Retracted: No

PubPeer comments:
 Figure 1 of 10.1371 journal.pone.0060817 appears to have image overlaps with Figure 4A of 10.1158 1541-7786.MCR-13-0239, after rotation. As the first author appears to have left this lab, perhaps Dr. Morris could investigate that authoru2019s papers. I have found issues which each I have reviewed. ***  ***  ,
Association of MMP2 and MMP9 gene polymorphisms with the recurrent spontaneous abortion: A meta-analysis
Authors: Ying-Pu Sun
Yang Yan
Lanlan Fang
Yiping Yu
Yuxi Li
Yiran Li
Jung-Chien Cheng
Journal: Gene (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Matrix metalloproteinases; Meta-analysis; Recurrent spontaneous abortion; Single nucleotide polymorphisms.
Affiliations: Center for Reproductive Medicine, Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China., Center for Reproductive Medicine, Henan Key Laboratory of Reproduction and Genetics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. Electronic address: .

Abstract:  Background: Recurrent spontaneous abortion (RSA) accounts for the most common complication of early pregnancy in humans. Matrix metalloproteinases (MMPs) play important regulatory roles in implantation and placentation to ensure a successful pregnancy. Single nucleotide polymorphisms (SNPs) have been identified in the promoters of MMP2 and MMP9 genes. However, the associations between MMP2 and MMP9 SNPs and the RSA risk remain unclear. The aim of this meta-analysis was to investigate whether MMP2 (-735C&gt;T) and MMP9 (-1562C&gt;T) SNPs are associated with the risk of RSA. Methods: Literatures published before 17th April 2020 were screened to identify the eligible studies. Heterogeneity, sensitivity and publication bias analysis were analyzed by the STATA software. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the Review Manager software with fixed effects model. Results: After screening, 2 studies for MMP2 (-735C&gt;T) (278 RSA cases and 265 controls) and 4 studies for MMP9 (-1562C&gt;T) (520 RSA cases and 512 controls) were enrolled in this meta-analysis. Results showed that MMP2 (-735C&gt;T) presented a statistically significant association with the risk of RSA under allelic (T vs C: OR = 1.50, 95% CI = 1.14-1.98, P = 0.004, I2 = 31%), heterozygote (CT vs CC: OR = 1.74, 95% CI = 1.22-2.50, P = 0.003, I2 = 41%) and dominant (TT + CT vs CC: OR = 1.74, 95% CI = 1.23-2.45, P = 0.002, I2 = 40%) genetic models. MMP9 (-1562C&gt;T) in allelic (T vs C: OR = 1.34, 95% CI = 1.08-1.65, P = 0.007, I2 = 0%), heterozygote (CT vs CC: OR = 1.38, 95% CI = 1.06-1.79, P = 0.02, I2 = 0%) and dominant (TT + CT vs CC: OR = 1.41, 95% CI = 1.10-1.82, P = 0.008, I2 = 0%) genetic models were significantly correlated with the RSA risk. Conclusions: Our meta-analysis results suggest that MMP2 -735T allele and MMP9 -1562T allele have significant association with the risk of RSA. 

Retracted: No

PubPeer comments:
 The text refers to a  Begger s test , once in the Methods section and four times in Results. E.g. * The funnel plots and Beggeru2019s test were applied to assess the potential publication biases in allelic, heterozygote and dominant genetic models (Figure 4). No obvious asymmetry of Beggeru2019s test was observed in any comparisons *. Could the authors elaborate on this test? ,
Inhibition of Mcl-1 promotes senescence in cancer cells: implications for preventing tumor growth and chemotherapy resistance
Authors: Abeba Demelash
Elzbieta Bolesta
John C Papadimitriou
Dhan V Kalvakolanu
Mathew L Lesniewski
Simon E Schlanger
Brian R Gastman
Shreeram C Nallar
Lukas W Pfannenstiel
Megan Tobin
Journal: Molecular and cellular biology (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: senescence; oncogenesis; chemotherapy resistance; Mcl-1; CIS
Affiliations: Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA., Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA, Department of Biochemistry, Case Western Reserve University, Cleveland, Ohio, USA, Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA, Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA, Institutes of Head and Neck, Dermatology and Plastic Surgery, Taussig Cancer Center, Departments of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, USA

Abstract:  Although senescence in oncogenesis has been widely studied, little is known regarding the role of this process in chemotherapy resistance. Thus, from the standpoint of enhancing and improving cancer therapy, a better understanding of the molecular machinery involved in chemotherapy-related senescence is paramount. We show for the first time that Mcl-1, a Bcl-2 family member, plays an important role in preventing chemotherapy-induced senescence (CIS). Overexpression of Mcl-1 in p53‚Å?cell lines inhibits CIS. Conversely, downregulation of Mcl-1 makes cells sensitive to CIS. Surprisingly, downregulation of Mcl-1 in p53‚Å?cells restored CIS to similar levels as p53‚Å?cells. In all cases where senescence can be induced, we observed increased p21 expression. Moreover, we show that the domain of Mcl-1 responsible for its antisenescent effects is distinct from that known to confer its antiapoptotic qualities. In vivo we observe that downregulation of Mcl-1 can almost retard tumor growth regardless of p53 status, while overexpression of Mcl-1 in p53‚Å?cells conferred resistance to CIS and promoted tumor outgrowth. In summary, our data reveal that Mcl-1 can inhibit CIS in both a p53-dependent and -independent manner in vitro and in vivo and that this Mcl-1-mediated inhibition can enhance tumor growth in vivo. 

Retracted: No

PubPeer comments:
 Figure 5C appears to have a repeated image. ***  ,
Low expression of miR-30a-5p induced the proliferation and invasion of oral cancer via promoting the expression of FAP
Authors: Zezhang Tao
Aili Tan
Peng Ruan
Journal: Bioscience Reports (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: FAP; Oral cancer; miR-30a-5p.
Affiliations: Department of Oncology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, P.R. China., Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, P.R. China ., Department of Obstetrics & Gynecology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, P.R. China .

Abstract:  The study aimed at investigating the effects of miR-30a-5p on the biological functions of oral cancer cells and figuring out the potential mechanism. We first verified the low expression of miR-30a-5p and high expression of FAP (Homo sapiens fibroblast activation protein Œ±) in oral cancerous tissues and their negative correlation. Then, the target relationship between miR-30a-5p and FAP was validated by dual luciferase reporter assay and biotin-coupled miRNA pulldown assay. After transfection in Tca-8113 cells and SCC-15 cells, MTT, colony formation, Transwell, and wound healing assays were performed to investigate how miR-30a-5p and FAP adjusted propagation, invasiveness, and migration, respectively. Mounting evidence supported that miR-30a-5p directly targetted FAP and suppressed its expression in oral cavity cancer cells (OSCCs). By suppressing FAP expression, miR-30a-5p significantly inhibited cell propagation, migration, and invasion. Therefore, miR-30a-5p might be a new therapeutic target for oral cancer treatment. 

Retracted: No

PubPeer comments:
 Fig 1F, the blots seems to have traces of splicing  Fig 4B, two same images  ,
Effect of TGF-Œ≤1 on myocardial cell apoptosis in rats with acute myocardial infarction via MAPK signaling pathway
Authors: C-B Lei
J Jiang
Y Wei
X-G Zhang
L Wang
H-Y Liang
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: TGF-Œ≤1; myocyte hypertrophy; ventricular remodeling; myocardial infarction; mRNA
Affiliations: Department of Clinical Laboratory, Affiliated Hospital of Weifang Medical College, Weifang, China. .

Abstract:  Objective: Transforming growth factor beta 1 (TGF-Œ≤1) can promote myocyte hypertrophy, thus playing an important role in ventricular remodeling after myocardial infarction (MI). Materials and methods: In this study, the model of MI was established in rats through ligating the left anterior descending coronary artery. Subsequently, the messenger ribonucleic acid (mRNA) and protein expression levels of TGF-Œ≤1 in myocardial cells in both model group and sham operation group were determined. The effects of TGF-Œ≤1 treatment on myocardial cell apoptosis in MI rats were explored. Moreover, the changes of mitogen-activated protein kinase (MAPK) signaling pathway in rats with acute MI were verified. In addition, the protein expressions of phosphorylated-MAPK kinases 3/6 (p-MKK3/6) and MKK3/6 in myocardial cells of the two groups were analyzed. Results: The mRNA and protein expression levels of TGF-Œ≤1 in myocardial cells of acute MI rats were significantly higher than those in the sham operation group (p&lt;0.01). After treatment with TGF-Œ≤1, the expression level of B-cell lymphoma 2 (Bcl-2) associated X protein (Bax) was obviously down-regulated. The Bax/Bcl-2 ratio was notably lower than that in control group (p&lt;0.01). Meanwhile, the proportion of apoptotic cells decreased remarkably (p&lt;0.01). In the model group, no evident change was observed in the protein expression level of MKK3/6, whereas the levels of p-MKK3/6 were prominently up-regulated (p&lt;0.01). Conclusions: TGF-Œ≤1 can activate MKK3/6 in the MAPK signaling pathway to resist the apoptosis of myocardial cells in acute MI rats. 

Retracted: No

PubPeer comments:
 Fig 2B  Protein expression of TGF-u03b21 in myocardial cells ; Fig 3 A, B,  Expression levels of Bax and Bcl-2 after treatment with TGF-u03b21 ; and Figure 4.  Protein expressions of MKK3 6 and p-MKK3 6 in myocardial cells of the two groups .  The loading controls are replicated so well, they could almost be duplicates. ,
Retracted : microRNA‚Ä?83 suppresses the PI3K‚ÄêAKT‚ÄêMTOR signaling pathway to inhibit development of cervical cancer via down‚Äêregulating PARP2
Authors: Yan Jiao
Min Hao
Peng Teng
Xin Tang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PARP2; PI3K-AKT-MTOR signaling pathway; apoptosis; cervical cancer; invasion
Affiliations: Department of Gynecology and Obstetrics, The Second Hospital of Shanxi Medical University, Taiyuan, P. R. China., Department of Gynecology and Obstetrics, Xuzhou Central Hospital, Xuzhou, P. R. China.

Abstract:  This study aims to evaluate the effect of the regulatory relationship between microRNA-383 (miR-383) and PARP2 in the cell migration and invasion in human with cervical cancer (CC) via the PI3K-AKT-MTOR signaling pathway. Cancerous tissues and corresponding paracancerous tissues were collected from 115 patients with CC. The positive expression rate of PARP2 was detected by immunohistochemistry. HeLa cells with highest miR-383 expression were selected and assigned into the blank, negative control (NC), miR-383 mimic, miR-383 inhibitor, si-PARP2, and miR-383 inhibitor + si-PARP2 groups. qRT-PCR and Western blot were performed to evaluate the expression of miR-383, PI3K, AKT, mTOR, PARP2, and p70S6K. MTT assay were utilized to measure cell viability. Transwell assay were applied to evaluate cell invasion and metastasis. Dual luciferase reporter assay identified that PARP2 is a target gene of miR-383. Cancerous tissues manifested higher expression of PI3K, AKT, mTOR, PARP2, and p70S6K but lower miR-383 expression than paracancerous tissues. Compared with the blank and NC groups, the miR-383 mimic and si-PARP2 groups had decreased expression of PI3K, AKT, mTOR, PARP2, and p70S6K mRNA and protein. In the miR-383 mimic and si-PARP2 groups, the cell viability, migration, and invasion were descended, in comparison to the blank and NC groups. All above parameters showed an opposite trend in the miR-383 inhibitor group when compared with the blank and NC groups. This study demonstrates that miR-383 could down-regulate PARP2 to protect against CC by inhibiting PI3K-AKT-MTOR signaling pathway. 

Retracted: Yes

PubPeer comments:
 Overlapping segments in three panels are shown by colored boxes.  , 
 #1 Here comparing **two** panels of Fig 4 *[below]*, with rotated Fig 3C from [Banerjee et al (2015)] *[above]*.  , 
 #3 The resemblance is relevant since both figures belong to the same anatomical structure. Histologically, they may seem similar which is based on the perception of the observer. I think no further reconciliation is necessary. Thanks Sushant , 
 As it was promising from the previous comments of #1 and #3, I tried a reconstruction of the original view based on a SIFT keypoint detection algorithm. Voilu00e0  , 
 #1 @ Brachystegia Boehmii There is no overlapping segment in the three panels as indicated. I believe it is a difference in perception of the observer which has occurred since the panels belong to the same anatomical structure. I do not accept your opinion on the same. Thanks Sushant ,
Characterisation of the sites of DNA damage-induced 53BP1 phosphorylation catalysed by ATM and ATR
Authors: Hilary McLauchlan
Rachel Toth
C James Hastie
Paul Jowsey
Nicholas A Morrice
John Rouse
Journal: DNA Repair (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 53BP1; tumour suppressor; genome stability; phosphorylation; ionising radiation
Affiliations: MRC Protein Phosphorylation Unit, Sir James Black Centre, University of Dundee, Dundee, Scotland, UK.

Abstract:  The 53BP1 tumour suppressor, an important regulator of genome stability, is phosphorylated in response to ionising radiation (IR) by the ATM protein kinase, itself an important regulator of cellular responses to DNA damage. The only known sites of phosphorylation in 53BP1 are Ser25 and/or Ser29 but 53BP1 lacking these residues is still phosphorylated after DNA damage. In this study, we use mass spectrometry-based together with bioinformatic analysis to identify novel DNA damage-regulated sites of 53BP1 phosphorylation. Several new sites were identified that conform to the consensus Ser/Thr-Gln motif phosphorylated by ATM and related kinases. Phospho-specific antibodies were raised, and were used to demonstrate ATM-dependent phosphorylation of these residues in 53BP1 after exposure of cells to IR. Surprisingly, 53BP1 was also phosphorylated on these residues after exposure of cells to UV light. In this case, 53BP1 phosphorylation did not require ATM but required ATR instead. These data reveal that 53BP1 is phosphorylated on multiple residues in response to different types of DNA damage, and that 53BP1 is regulated by ATR in response to UV-induced DNA damage. 

Retracted: No

PubPeer comments:
 Could the authors explain the identical sequence of primers for the microRNA 503 in mice in another paper?  , 
 #1 Thanks for your comments on our paper. Having double-checked our primer ordering records, we found that the Mir-26a RT primer sequence is correct. The sequence repeated with another paper is the stem loop structure used for microRNA reverse transcription primer. The next few bases u201cAGCCTATu201d are specific for miR-26a. However, we also found that we wrote the F and R primers of miR-26a wrong in the paper, and the correct primer sequence is as follows. Mm-Mir26a-F GCGGTTCAAGTAATCCAGG Mm-Mir26a-R TGTCGTGGAGTCGGCAATT We kept our primer ordering records at that time, which confirmed that our data and conclusion are correct. We would like to expression our sincere and serious apology to you and to the journal for the accidental mistake and any inconvenience the mistake may cause. ,
Fluid‚ÄìStructure Interaction-Based Biomechanical Perception Model for Tactile Sensing
Authors: Zheng Wang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: haptic interfaces; tactile sensation; tactile biomechanics; tactile perception; design

Abstract:  The reproduced tactile sensation of haptic interfaces usually selectively reproduces a certain object attribute, such as the object's material reflected by vibration and its surface shape by a pneumatic nozzle array. Tactile biomechanics investigates the relation between responses to an external load stimulus and tactile perception and guides the design of haptic interface devices via a tactile mechanism. Focusing on the pneumatic haptic interface, we established a fluid-structure interaction-based biomechanical model of responses to static and dynamic loads and conducted numerical simulation and experiments. This model provides a theoretical basis for designing haptic interfaces and reproducing tactile textures. 

Retracted: Yes

PubPeer comments:
 2019 retraction notice. https: journals.plos.org plosone article?id=10.1371 journal.pone.0079472 ,