PReD-Bench/PRed-Bench huggingface dataset:
Erythropoietin promotes the growth of pituitary adenomas by enhancing angiogenesis
Authors: Xuanmin Gu
Jinsheng Yang
Tao Li
Zheng Xiao
Bo Fan
Journal: International Journal of Oncology (2012)
Discipline: CLINICAL MEDICINE
Keywords: rhEPO; pituitary adenomas; tumor growth; angiogenesis; EPOR negative
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, PR China.

Abstract:  rhEPO is frequently used in clinical practice to treat anemia. However, recently rhEPO has been reported to accelerate tumor growth, progression and metastasis. Many pituitary adenoma patients, particularly those with macroprolactinomas, tend to have anemia and may need rhEPO therapy. To date, whether rhEPO has deleterious effects on pituitary adenomas has not been defined. Here we demonstrated for the first time that human pituitary adenomas are EPOR negative tumors and rhEPO accelerated the tumor growth of MMQ pituitary adenoma xenografts via enhancement of angiogenesis in vivo, whereas rhEPO displayed no direct effect on MMQ cells in vitro. Our mechanistic study showed that rhEPO administration increased phosphorylation of JAK2, STAT3 and VEGF expression in human umbilical vein endothelial cells (HUVECs) in vitro and in MMQ cell xenografts in vivo. Furthermore, VEGF inhibitor attenuated rhEPO induced angiogenesis and delayed tumor growth in MMQ pituitary adenoma xenografts in vivo. JAK2 inhibitor AG490 attenuated EPO induced HUVECs proliferation, phosphorylation of JAK2, STAT3 and VEGF upregulation in vitro and inhibited EPO induced vessel formation in Chicken chorioallantoic membrane (CAM) angiogenesis model in vivo. These results suggest that rhEPO administration may promote the growth of pituitary adenomas by enhancing angiogenesis through EPO-JAK2-STAT3-VEGF signaling pathway. rhEPO should be used with caution in anemia patients bearing pituitary adenoma due to its potential deleterious effects. 

Retracted: No

PubPeer comments:
 image duplication contradicts legend ![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. ,
LncRNA Gm5091 alleviates alcoholic hepatic fibrosis by sponging miR-27b/23b/24 in mice
Authors: Bo Zhou
Wenwen Yuan
Xinping Li
Journal: Cell Biology International (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RNA interaction; alcoholic hepatic fibrosis; hepatic stellate cell activation; lncRNA Gm5091; miR-27b/23b/24.
Affiliations: College of Veterinary Medicine; Northwest A&F University; Yangling Shaanxi 712100 China

Abstract:  The regulatory roles of lncRNAs in the development of alcoholic hepatic fibrosis (AHF) have not been revealed. Here, we found lncRNA Gm5091 was being downregulated in mouse hepatic stellate cells (HSCs) during AHF. Then, Gm5091 was, respectively, overexpressed and knocked down in alcohol-treated primary HSCs. Our results showed that Gm5091 negatively regulated cell migration, ROS content, IL-1β secretion, and expression of Collagen I and markers of HSC activation including α-SMA and Desmin. Furthermore, bioinformatics analysis showed that Gm5091 sequence contained binding sites of miR-27b, miR-23b, and miR-24, and we proved that miR-27b/23b/24 all bound to Gm5091 by using RNA pull-down assay. Full-length Gm5091 could decrease the miR-27b/23b/24 levels, but the truncated Gm5091 deleting the binding sites could not. Finally, we confirmed that full-length Gm5091 could alleviate AHF in vivo, but the truncated Gm5091 could not. In conclusion, lncRNA Gm5091 alleviates mouse AHF by sponging miR-27b/23b/24. 

Retracted: No

PubPeer comments:
 In Figure 5H, two micrographs have been duplicated, manipulated and presented as something else. ![file] ,
ALA-mediated biphasic downregulation of α-7nAchR/HIF-1α along with mitochondrial stress modulation strategy in mammary gland chemoprevention
Authors: Shreesh Raj Sammi
Rakesh Pandey
Manjari Singh
Subhadeep Roy
Gaurav Kaithwas
Journal: Journal of cellular physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Caenorhabditis elegans; N-methyl- N-nitrosourea; breast cancer; mitochondria-mediated death apoptosis; ɑ-linolenic acid.
Affiliations: Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Lucknow, India., Department of Microbial Technology and Nematology, CSIR-Central Institute of Medicinal and Aromatic Plants, Lucknow, India.

Abstract:  The study elucidates the effect of ɑ-linolenic acid (ALA) on mitochondrial stress, hypoxic cancer microenvironment, and intervention of cholinergic anti-inflammatory pathway using N-methyl-N-nitrosourea (MNU) induced estrogen receptor (ER+) mammary gland carcinoma and Caenorhabditis elegans model, respectively. The efficacy of ALA was scrutinized in vivo and in vitro using various experiments like hemodynamic studies, morphological analysis, antioxidants parameters, immunoblotting, and quantitative reverse transcription polymerase chain reaction. The effect of ALA was also validated using C. elegans worms. ALA administration had a positive effect on tissue architecture of the malignancy when scrutinized through the whole mount carmine staining, hematoxylin and eosin staining, and scanning electron microscopy. The proteomic and genomic checkpoint revealed the participation of mitochondrial dysfunction, alteration of hypoxic microenvironment, and involvement of cholinergic anti-inflammatory response after treatment with ALA. ALA treatment has also increased the level of synaptic acetylcholine and acetylcholine esterase with a significant decrease in lipid content. It was concluded that ALA persuaded the mitochondrial stress, activation of downstream cholinergic anti-inflammatory markers, and favorable regulation of hypoxia microenvironment through inhibition of fatty acid synthase and sterol regulatory element-binding protein. 

Retracted: No

PubPeer comments:
 Is this image recycling? ![file] , 
 Authors have published an erratum for the same. https: onlinelibrary.wiley.com doi full 10.1002 jcp.29257 ,
Downregulation of monocarboxylate transporter 1 inhibits the invasion and migration through suppression of the PI3K/Akt signaling pathway in human nasopharyngeal carcinoma cells
Authors: Fang Liu
Xiaojin Sun
Fang Fang
Jiao Gao
Pei Zhang
Surong Zhao
Hao Liu
Jie Ma
Journal: Journal of Bioenergetics and Biomembranes (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Invasion; MCT1; Migration; Nasopharyngeal carcinoma; PI3K/Akt signaling pathway.
Affiliations: School of Pharmacy, Bengbu Medical College, Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, Bengbu, 233030, Anhui, People's Republic of China., Department of Orthopedics, the First Affiliated Hospital f Bengbu Medical College, Bengbu, 233004, Anhui, People's Republic of China., School of Pharmacy, Bengbu Medical College, Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, Bengbu, 233030, Anhui, People's Republic of China. .

Abstract:  Monocarboxylate transporter 1 (MCT1) has been reported to be correlated wtih decreased survival and advanced stage of progression in a series of human tumor cells and primary cancers. Specifically, MCT1 has been documented to be involved in tumor progression, including invasion and migration. Here, we investigated the mechanism and effect of regulation of MCT1 on invasion and migration of nasopharyngeal carcinoma (NPC) cells. In the study, we firstly demonstrated that the expression of MCT1 in CNE2Z cells was obviously higher than that in HNE1 cells. Downregulation of MCT1 inhibited the invasion and migration in CNE2Z cells, upregulated the expression of E-cadherin, TIMP (tissue inhibitor of metalloproteinase)-2 and TIMP-1, and suppressed the expression of matrix metalloproteinases (MMP)-9 and MMP-2. Correspondingly, upregulation of MCT1 enhanced the invasive and migratory potential in HNE1 cells, increased the expression of MMP-9 and MMP-2, and downregulated the expression of E-cadherin, TIMP-2 and TIMP-1. The mechanistic study demonstrated that the effect of MCT1 might be correlated with PI3K/Akt signaling pathway. LY294002, a PI3K inhibitor, increased the inhibition of invasion and migration mediated by downregulation of MCT1 in CNE2Z cells. These findings collectively suggested that MCT1 might act as a new regulator to improve invasion and migration of NPC cells and be correlated with activating the PI3K/Akt pathway. 

Retracted: No

PubPeer comments:
 Fig. 6b contains two images which appear to overlap. ![file] , 
 There are other images in this paper which appear to overlap. TAM. An example from Figure 3a: *** ![file] ,
Luteinizing hormone-releasing hormone peptide tethered nanoparticulate system for enhanced antitumoral efficacy of paclitaxel
Authors: Raksha Ghanghoria
Narendra Kumar Jain
Krishna Chuttani
Rakesh Kumar Tekade
Anil Kumar Mishra
Journal: Nanomedicine (2016)
Discipline: CLINICAL MEDICINE
Keywords: LHRH; PLGA copolymer; biodistribution; cancer targeting; paclitaxel
Affiliations: Pharmaceutics Research Laboratory, Department of Pharmaceutical Sciences, Dr. Hari Singh Gour University, Sagar 470003 MP, India., The University of Texas Southwestern Medical Center, Advanced Imaging Research Centre, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA., Division of Cyclotron & Radiopharmaceutical Sciences, Molecular Imaging Research Center, Institute of Nuclear Medicine & Allied Sciences (INMAS), DRDO, 110054 Delhi, India.

Abstract:  Aim: Paclitaxel (PTX) is an effective anticancer agent used in the therapy of a wide variety of cancers. However, the drug is difficult to formulate due to its low solubility, and therefore, it is administered under slow infusion with castor oil/ethanol solution as surfactant that causes serious side effects. This investigation investigates leutinizing hormone releasing hormone (LHRH)-tethered nanparticulate system as modality for cancer-specific delivery of PTX and therefore minimizing the adverse effects. Materials &amp; methods: LHRH-tethered poly(lactic-co-glycolic acid) copolymer with poly ethylene glycol side chain was synthesized, characterized and employed to formulate PTX-loaded nanoparticulate system. Results &amp; conclusion: The developed nanoparticulate appears to be proficient in carrying as well as targeted delivery of PTX with improved therapeutic efficacy and better safety. 

Retracted: No

PubPeer comments:
 Areas indicated by circles show strange similarity . Please explain. ![file] ![file] , 
 ![file] Completely agreed with Grosourdya Appendiculata. There is no x-axis values and integrations in Fig 4A, while proton integration in Fig 4B is completely incorrect. Authors must clarify and provide a raw FID file for these NMR spectra. ,
MITF and PU.1 inhibit adipogenesis of ovine primary preadipocytes by restraining C/EBPβ
Authors: JunJie Hu
Yong Zhang
ChongMei Ruan
XingXu Zhao
Xiu Li
Journal: Cellular & molecular biology letters (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Adipogenesis; CCAAT-enhancer-binding protein-β; Lineage-specific transcription factor; Microphthalmia-associated transcription factor; PU box-binding protein.
Affiliations: College of Veterinary Medicine, Gansu Agriculture University, Lanzhou, 730070 China., College of Animal Science and Technology, Anhui Agriculture University, Hefei, 230036 China.

Abstract:  Background: PU box-binding protein (PU.1) is a master gene of hematopoietic lineage and an important specific transcription factor in osteoclast lineage. There is proof of its expression in adipose tissue, and it is known to significantly and negatively affect adipogenesis. However, it is unclear whether there are any other molecules involved in this process. Methods: We wished to explore the effect of PU.1's co-activator microphthalmia-associated transcription factor (MITF) on the adipogenic differentiation of ovine primary preadipocytes. The expression vectors pcDNA-MITF and pcDNA-PU.1, and MITF siRNA and PU.1 siRNA were transfected or co-transfected into ovine tail primary preadipocytes. Real-time PCR and western blot analysis were applied to investigate the expression levels of PU.1 and MITF. The morphologic changes in the cells were observed under a microscope at a magnification of × 200 after staining with Oil Red O. The triglyceride (TG) content in cells was also determined after transfection. Results: MITF and its co-activator PU.1 synergistically exhibited an opposite expression pattern to that of CCAAT-enhancer-binding protein-β (C/EBPβ) during adipogenic differentiation of ovine primary preadipocytes. Before induction of differentiation, overexpression of MITF or PU.1 inhibited the expression of C/EBPβ and adipogenesis in the cells; and knockdown of MITF or PU.1 promoted the expression of C/EBPβ and adipogenesis in the cells. The inhibitory or promotive effect was enhanced when MITF and PU.1 were co-overexpressed or co-silenced. However, when MITF and/or PU.1 were overexpressed after day 2 of differentiation, no changes in adipogenesis of the cells were observed. Conclusions: MITF and its co-activator PU.1 inhibited adipogenesis of ovine primary preadipocytes by restraining C/EBPβ. 

Retracted: No

PubPeer comments:
 Figure 2b appears to have two images which overlap. Although the wrong image could have been selected during upload, it isnu2019t clear how that would explain the difference in magnification. *** ![file] *** ![file] ,
Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition
Authors: Ting Sun
Xiaorong Yang
Xin Liu
Ming Ma
Binbin Gong
Qiang Chen
Wenjie Xie
Jie Chen
Journal: Oncology Letters (2019)
Discipline: CLINICAL MEDICINE
Keywords: epithelial-mesenchymal transition; gastric carcinoma proliferation enhancing transcript 1; lncRNAs; migration; proliferation
Affiliations: Department of Urology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330000, P.R. China., Department of Blood Transfusion, Jiangxi Provincial Children's Hospital, Nanchang, Jiangxi 330000, P.R. China.

Abstract:  Long non-coding RNAs (lncRNAs) have been demonstrated to serve vital roles in renal cell carcinoma (RCC) development. Gastric carcinoma high expressed transcript 1 (GHET1) regulates numerous biological processes in cancer cells. However, the biological role of GHET1 in RCC has not yet been identified. This study aimed to investigate the role of GHET1 in RCC. In the present study, the expression of GHET1 in RCC tissues and the 786-O, A498 and 293 cell lines was assessed by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, colony formation and cell scratch assays were used to determine the effects of GHET1 on tumorigenesis. Western blotting was performed to examine the effect of GHET1 on epithelial-mesenchymal transition (EMT) in RCC cells. GHET1 expression was significantly increased in the RCC samples in comparison with adjacent tissues. High expression levels of GHET1 were associated with distant metastasis and clinical stage severity, thus, high GHET1 expression may serve as a predictor for a poor prognosis. In addition, RCC cells presented higher GHET1 mRNA and protein expression levels compared with in 293 cells. Furthermore, silencing GHET1 suppressed cell growth, weakened cell migration and inhibited EMT of RCC cells in vitro. In conclusion, the present study suggested that GHET1 may be considered a therapeutic target for the treatment or prevention of RCC. 

Retracted: No

PubPeer comments:
 The colony forming assays in Figure 3 appear to be images cropped from only two wells. I have highlighted the overlaps below, except for the panel I have labelled  4 , where the overlap is difficult to see. ![file] We can reassamble parts of the original images to demonstrate that all of the images come from the same two colony forming assays. Note that the cropped images have been slightly stretched, consequently distorting the overall shape of the circular well somewhat. ![file] ,
12-Epi-Napelline Inhibits Leukemia Cell Proliferation via the PI3K/AKT Signaling Pathway In Vitro and In Vivo
Authors: Jia Han
Jian-Cai Tang
Bi-Qing Cai
Wei Hou
Fan Zhang
Journal: Evidence-based Complementary and Alternative Medicine (2021)
Discipline: CLINICAL MEDICINE
Keywords: 12-epi-napelline; leukemia cells; inhibitory effect; cell cycle arrest; apoptosis
Affiliations: School of Pharmacy, North of Si Chuan Medical College, Nan Chong, Si Chuan, China, Basic Medical College, North of Si Chuan Medical College, Nan Chong, Si Chuan, China

Abstract:  This study aimed to investigate the inhibitory effect of 12-epi-napelline on leukemia cells and its possible mechanisms. The inhibitory effects of 12-epi-napelline on K-562 and HL-60 cells were evaluated using the CCK-8 assay, cell cycle arrest and apoptosis were detected by flow cytometry, and the expression of related proteins was measured by western blot. A K-562 tumor model was established to evaluate the antitumor effect of 12-epi-napelline in vivo. A reduction in leukemia cell viability was observed after treatment with 12-epi-napelline. It was determined that the cell cycle was arrested in the G0/G1 phase, and the cell apoptosis rate was increased. Moreover, caspase-3 and Bcl-2 were downregulated, whereas cleaved caspase-3 and caspase-9 were upregulated. Further study revealed that 12-epi-napelline could suppress the expression of PI3K, AKT, p-AKT, and mTOR. Insulin-like growth factor 1 (IGF-1) attenuated 12-epi-napelline-induced apoptosis and ameliorated the repression of PI3K, AKT, p-AKT, and mTOR by 12-epi-napelline. Animal experiments clearly showed that 12-epi-napelline inhibited tumor growth. In conclusion, 12-epi-napelline restrained leukemia cell proliferation by suppressing the PI3K/AKT/mTOR pathway in vitro and in vivo. 

Retracted: No

PubPeer comments:
 Fig. 3e top panel of HL-60 looks like having 5 blobs, while all the others having 4. Any explanation from the authors? ![file] , 
 mTOR in Fig. 4a and P-AKT in Fig. 4c look strikingly similar. Explanation? ![file] , 
 Fig. 5e. PI3K and AKT panels are unusually similar to each other, after vertically stretching PI3K. ![file] , 
 #3 The first author provides the two original images ![](http: ![file] ![file] ) According to the original images, we think the first author may make a mistake in the experiment. The two images may be produced due to the different exposure time. We further checek the AKT original image. we found the image of AKT expression is error. We provide the New image of AKT expression. #2mTOR in Fig. 4a and P-AKT in Fig. 4c look strikingly similar. We checked the original data. We found the first author had made a mistake due to our careless during the editional of pictures. The image of P-AKT in Fig. 4c is error .We will provide the new original image. We will re-experiment and ensure the results. After that ,we will contact the editor and correct our errors. #1 Thank you for your attention. When I have received the E-mail, I have quired the first author and check the original image. Fig3e : It has four blots. she provided the original image.![](http: ) ![file] , 
 #3 #3 ![file] ,
The H1 histamine receptor regulates allergic lung responses
Authors: Clinton B Mathias
Hans C Oettgen
Krista L Harrison
Paul J Bryce
Takeshi Watanabe
Raif S Geha
Journal: Journal of Clinical Investigation (2006)
Discipline: CLINICAL MEDICINE
Keywords: Histamine; H1R; Th2 cytokines; allergic inflammation; asthma model
Affiliations: Division of Immunology, Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA. 

Abstract:  Histamine, signaling via the type 1 receptor (H1R), has been shown to suppress Th2 cytokine production by in vitro cultured T cells. We examined the role of H1R in allergic inflammation in vivo using a murine asthma model. Allergen-stimulated splenic T cells from sensitized H1R-/- mice exhibited enhanced Th2 cytokine production. Despite this Th2 bias, allergen-challenged H1R-/- mice exhibited diminished lung Th2 cytokine mRNA levels, airway inflammation, goblet cell metaplasia, and airway hyperresponsiveness (AHR). Restoration of pulmonary Th2 cytokines in H1R-/- mice by intranasal IL-4 or IL-13 restored inflammatory lung responses and AHR. Further investigation revealed that histamine acts as a T cell chemotactic factor and defective T cell trafficking was responsible for the absence of lung inflammation. Cultured T cells migrated in response to histamine in vitro, but this was ablated by blockade of H1R but not H2R. In vivo, allergen-specific WT but not H1R-/- CD4+ T cells were recruited to the lungs of naive recipients following inhaled allergen challenge. H1R-/- T cells failed to confer airway inflammation or AHR observed after transfer of WT T cells. Our data establish a role for histamine and H1R in promoting the migration of Th2 cells into sites of allergen exposure. 

Retracted: No

PubPeer comments:
 The authors in this paper considered the notion of u201c**dual hesitant q-rung orthopair fuzzy numbers**u201d, proposed some operators, called **Hamacher aggregation operators**, and applied them to multiple attribute decision making. This paper is very similar to the paper by G.W. Wei and M Lu published in 2017 (doi: 10.1515 acsc-2017-0024) where **dual hesitant Pythagorean fuzzy numbers** and their **Hamacher aggregation operators** were considered. See comment for the 2017 paper (doi: 10.1515 acsc-2017-0024) on https: pubpeer.com publications ABC44FFC329A297A2B8E40B23B37AD Actually, by replacing the parameter **$q=2$ (Pythagorean)** by **a general value (q-rung orthopair)**, every notion and formula in the 2017 paper would correspond to the notion and formula in this 2019 paper. Besides, like the case for the 2017 paper, the results presented in this paper make no sense too. For example, Because the numbers of values change for the operations $otimes$ and $oplus$ in Definition 6 and Definition 7, **Property 1 (idempotency) in eq.(12) simply does not hold for DHq-ROHWA operator** although the authors claimed that it can be easily proved. ![file] ![file] ![file] , 
 A typical citation pattern of GW Wei, the second author of this paper. ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ![file] ,
Cow milk induced allergies (CMA) and asthma in new born
Authors: J-F Liu
H-W Wu
W Wang
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cow milk; allergies; asthma; newborn; withdrawn
Affiliations: Department of Neonatology, Xuzhou Children's Hospital, Xuzhou, Jiangsu, P.R. China.

Abstract:  The article "Cow milk induced allergies (CMA) and asthma in new born" by W. Wang, H.-W. Wu, J.-F. Liu, published in Eur Rev Med Pharmacol Sci 2016; 20 (6): 1008-1014 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
KSR1 regulates BRCA1 degradation and inhibits breast cancer growth
Authors: J Stebbing
H Zhang
K Blighe
A R Green
Y Xu
I O Ellis
M Periyasamy
H J Lenz
L C Lit
A Grothey
Y Lombardo
W Zhang
G Giamas
J A Shaw
Journal: Oncogene (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: KSR1; breast cancer; tumor suppressor; BRCA1; BARD1
Affiliations: Division of Cancer, Department of Surgery and Cancer, Imperial College London, Imperial College Centre for Translational and Experimental Medicine, Hammersmith Hospital Campus, London, UK., 1] Division of Cancer, Department of Surgery and Cancer, Imperial College London, Imperial College Centre for Translational and Experimental Medicine, Hammersmith Hospital Campus, London, UK [2] Faculty of Medicine, Department of Physiology, University of Malaya, Kuala, Lumpur, Malaysia., Department of Cellular Pathology, Queen's Medical Centre, Nottingham University Hospital NHS Trust, Nottingham, UK., Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester, UK., Division of Medical Oncology, University of Southern California, Norris Comprehensive Cancer Centre, Keck School of Medicine, Los Angeles, CA, USA., Faculty of Medicine, Department of Physiology, University of Malaya, Kuala, Lumpur, Malaysia.

Abstract:  Kinase suppressor of Ras-1 (KSR1) facilitates signal transduction in Ras-dependent cancers, including pancreatic and lung carcinomas but its role in breast cancer has not been well studied. Here, we demonstrate for the first time it functions as a tumor suppressor in breast cancer in contrast to data in other tumors. Breast cancer patients (n&gt;1000) with high KSR1 showed better disease-free and overall survival, results also supported by Oncomine analyses, microarray data (n=2878) and genomic data from paired tumor and cell-free DNA samples revealing loss of heterozygosity. KSR1 expression is associated with high breast cancer 1, early onset (BRCA1), high BRCA1-associated ring domain 1 (BARD1) and checkpoint kinase 1 (Chk1) levels. Phospho-profiling of major components of the canonical Ras-RAF-mitogen-activated protein kinases pathway showed no significant changes after KSR1 overexpression or silencing. Moreover, KSR1 stably transfected cells formed fewer and smaller size colonies compared to the parental ones, while in vivo mouse model also demonstrated that the growth of xenograft tumors overexpressing KSR1 was inhibited. The tumor suppressive action of KSR1 is BRCA1 dependent shown by 3D-matrigel and soft agar assays. KSR1 stabilizes BRCA1 protein levels by reducing BRCA1 ubiquitination through increasing BARD1 abundance. These data link these proteins in a continuum with clinical relevance and position KSR1 in the major oncoprotein pathways in breast tumorigenesis. 

Retracted: No

PubPeer comments:
null, 
null, 
 Additionally, the KSR1 blots are duplicated in the figures mentioned above but labelled as different cell types.![file] ,
miR-29b and miR-29c are involved in Toll-like receptor control of glucocorticoid-induced apoptosis in human plasmacytoid dendritic cells
Authors: Qianshan Tao
Jingpu Zhao
Yi Liu
Kaili Yan
Zhimin Zhai
Huiping Wang
Jianxian Wu
Xianshan Shen
Tianping Chen
Yongfeng Hong
Xiuli Kan
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Glucocorticoids; Toll-like receptor; plasmacytoid dendritic cells; apoptosis; microRNAs
Affiliations: Department of Rehabilitation, The Second Affiliated Hospital to Anhui Medical University, Economic Development Zone, Hefei City, Anhui, China.

Abstract:  Glucocorticoids (GCs) are frequently used to treat many of the acute disease manifestations associated with inflammatory and autoimmune disorders. However, Toll-like receptor (TLR) pathway-activated plasmacytoid dendritic cells (pDCs) are resistant to GC-induced apoptosis, which leads to the inefficiency of GCs in the treatment of type I interferon-related autoimmune diseases, such as systemic lupus erythematosus (SLE). Therefore, compounds promoting pDC apoptosis may be helpful for improving the efficacy of GCs. In this study, we performed screening to identify microRNAs (miRNAs) involved in TLR-inhibited GC-induced pDC apoptosis and found an array of miRNAs that may regulate pDC apoptosis. Among those demonstrating altered expression, 6 miRNAs were inhibited in TLR-activated pDCs. Bioinformatics analysis and functional studies indicated that miR-29b and miR-29c were 2 key miRNAs involved in TLR-inhibited GC-induced pDC apoptosis. Furthermore, both of these miRNAs promoted pDC apoptosis by directly targeting Mcl-1 and Bcl-2 in human primary pDCs. Our findings provide new targets that could improve the efficacy of GCs for the treatment of SLE. 

Retracted: No

PubPeer comments:
 Figure 5A * Red boxes: Two flow cytometry panels look remarkably similar, but have different measured percentages Reported to the journal in October 2015, but no action as of today. ![file] ,
Targeting PIN-1 Attenuates GCB DLBCL Cell Proliferation Through Inhibition of PI3K/AKT Signaling
Authors: Yang Gao
Luyao Zhao
Fuqiang Wang
Yufen Yuan
Mei Guo
Jia Li
Haijun Yang
Junkuo Li
Ping Zhang
Haimei Li
Jingfang Zhang
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: DLBCL; PI3K/AKT signaling pathway; PIN-1.
Affiliations: Department of Pathology, Anyang Tumor Hospital, The Fourth Affiliated Hospital of Henan University of Science and Technology, Anyang 455000, People's Republic of China., NHC Key Laboratory of Biotechnology of Antibiotics, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100032, People's Republic of China.

Abstract:  Introduction: Diffuse large B cell lymphoma (DLBCL) is a highly heterogeneous type of non-Hodgkin lymphoma with many molecular subtypes that can be distinguished by gene expression profiling (GEP). However, the pathogenesis of DLBCL is still unclear. Materials and methods: The expression levels of the prolyl isomerase PIN-1 and other related proteins were determined in 73 primary DLBCL patient samples and cell lines by Western blotting (WB) and immunohistochemical (IHC) staining. Cell cycle and apoptosis were evaluated by flow cytometry. Lymphoma cell viability was detected by CCK-8 proliferation assay. Results: High levels of PIN-1 expression were detected in 55% of germinal center B cell (GCB) DLBCL patient samples, whereas such abnormal expression levels were found in only 11% of non-GCB DLBCL patient samples. PIN-1 expression was positively associated with activation of the oncogenic phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway in both GCB DLBCL cell lines and primary patient samples. Depletion of PIN-1 was cytotoxic to GCB DLBCL model cell lines because it led to inhibition of the PI3K/AKT signaling pathway, revealing a GCB DLBCL subgroup that is dependent on this pathway. A PI3K inhibitor was selectively toxic to GCB DLBCL lines expressing high levels of PIN-1. Conclusion: Our study used PIN-1 to identify a new subgroup of GCB DLBCL associated with the PI3K/AKT signaling pathway, and our findings reveal that inhibition of PI3K is a promising therapeutic approach for GCB DLBCL. 

Retracted: No

PubPeer comments:
 In this study the authors are using the PI3K inhbitor LY294002, which is an inhibitor that has been abandoned due to lack of specificity. It is not without reason that no clinical studies with LY294002 are no longer registered. In addition, the authors are using LY294002 at an insane high concentration (5 mM)! During the stone age we used it at a concentration 5-20 microMolar... In FIgure 3B, it is clear that the Western immunoblots of p-AKT and AKT do not originate from the same gel experiment due to the difference in band shape. ![file] ,
miR‐17‐5p promotes proliferation and epithelial‐mesenchymal transition in human osteosarcoma cells by targeting SRC kinase signaling inhibitor 1
Authors: Yan Zhang
Xuefeng Zhao
Xiaoya Sun
Yadong Wang
Yuebai Li
Zhen Jia
Yisheng Wang
Hongya Guan
Yuan Ma
Yan Xu
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SRC kinase signaling inhibitor 1 (SRCIN1); epithelial-mesenchymal transition (EMT); microRNA-17-5p (miR-17-5p); osteosarcoma (OS).
Affiliations: Department of Biochemistry and Molecular Biology School of Basic Medical Sciences, Zhengzhou University Zhengzhou China, Department of Orthopaedic Surgery The First Affiliated Hospital of Zhengzhou University Zhengzhou China, Translational Medical Center, Zhengzhou Central Hospital Affiliated to Zhengzhou University Zhengzhou China

Abstract:  MicroRNA-17-5p (miR-17-5p) and epithelial-mesenchymal transition (EMT) have been reported to participate in the development and progression of multiple cancers. However, the relationship between the miR-17-5p and EMT in osteosarcoma (OS) is still poorly understood. This study was to investigate the effects of the miR-17-5p and its potential mechanism in regulating proliferation, apoptosis, and EMT of human OS. Quantitative real-time PCR was used to detect the miR-17-5p and SRC kinase signaling inhibitor 1 (SRCIN1) messenger RNA expression in OS specimens and cell lines. After transfection with miR-17-5p inhibitors, proliferation, apoptosis, migration, and invasion of OS cells were assessed by using the Cell Counting Kit-8, the annexin V-FITC apoptosis, wound-healing, and transwell assays. The SRCIN1 was validated as a target of the miR-17-5p through bioinformatics algorithms and luciferase reporter assay. Moreover, the expression of EMT markers, E-cadherin, N-cadherin, and Snail was identified by the Western blot analysis. MiR-17-5p was significantly upregulated in OS tumor samples and cell lines. It inhibited proliferation and EMT, and promoted apoptosis in OS. The SRCIN1 was identified as a direct target of the miR-17-5p. Silenced miR-17-5p could change the expression of EMT markers, such as upregulating the expression of E-cadherin, and downregulating the expression of N-cadherin and Snail through targeting the antioncogenic SRCIN1. These findings suggest that the miR-17-5p promotes cell proliferation, and EMT in human OS by directly targeting the SRCIN1, and reveal a branch of the miR-17-5p/SRCIN1/EMT signaling pathway involved in the progression of OS. 

Retracted: No

PubPeer comments:
 Figure 3 appears to include two images which overlap. *** ![file] , 
 #1 Please compare Fig 3B *[below]* with *[above]* 3C from [Sun et al (2018)] . ![] , 
 Please also compare the scratch-healing assay images (3A) from this paper *[right]* with *[left]* those from 3E of Sun et al. ![file] I ran out of colors but you get the idea. The recycling is admirable in its parsimony. , 
 As the authors do not appear interested in replying on this forum, I have notified the journal. , 
 The companion paper ([Sun et al 2018)] has undergone a correction. ,
Expression of ACE2, Soluble ACE2, Angiotensin I, Angiotensin II and Angiotensin-(1-7) Is Modulated in COVID-19 Patients
Authors: Jean-Louis Mege
Cléa Melenotte
Ikram Omar Osman
Matthieu Million
Christian A Devaux
Philippe Parola
Jean-Christophe Lagier
Line Meddeb
Andréas Stein
Didier Raoult
Philippe Brouqui
Bernard La Scola
Journal: Frontiers in Immunology (2021)
Discipline: IMMUNOLOGY
Keywords: ACE2 (Angiotensin Converting Enzyme-2); COVID-19; Hypertension; Renin – Angiotensin – Aldosterone System; SARS – CoV – 2.
Affiliations: Aix-Marseille Univ, IRD, APHM, MEPHI, IHU-Méditerranée Infection, Marseille, France., Aix-Marseille Univ, IRD, APHM, SSA, VITROME, IHU-Méditerranée Infection, Marseille, France., Centre National de la Recherche Scientifique (CNRS), Marseille, France.

Abstract:  The etiological agent of COVID-19 SARS-CoV-2, is primarily a pulmonary-tropic coronavirus. Infection of alveolar pneumocytes by SARS-CoV-2 requires virus binding to the angiotensin I converting enzyme 2 (ACE2) monocarboxypeptidase. ACE2, present on the surface of many cell types, is known to be a regulator of blood pressure homeostasis through its ability to catalyze the proteolysis of Angiotensin II (Ang II) into Angiotensin-(1-7) [Ang-(1-7)]. We therefore hypothesized that SARS-CoV-2 could trigger variations of ACE2 expression and Ang II plasma concentration in SARS-CoV-2-infected patients. We report here, that circulating blood cells from COVID-19 patients express less ACE2 mRNA than cells from healthy volunteers. At the level of circulating cells, this ACE2 gene dysregulation mainly affects the monocytes, which also show a lower expression of membrane ACE2 protein. Moreover, soluble ACE2 (sACE2) plasma concentrations are lower in prolonged viral shedders than in healthy controls, while the concentration of sACE2 returns to normal levels in short viral shedders. In the plasma of prolonged viral shedders, we also found higher concentrations of Ang II and angiotensin I (Ang I). On the other hand, the plasma levels of Ang-(1-7) remains almost stable in prolonged viral shedders but seems insufficient to prevent the adverse effects of Ang II accumulation. Altogether, these data evidence that the SARS-CoV-2 may affect the expression of blood pressure regulators with possible harmful consequences on COVID-19 outcome. 

Retracted: No

PubPeer comments:
 ![file] There are multiple undeclared splice sites in the immunoblots in Figure 4B and 4C. Apparently the bands were not from the same blots. Could authors provide an explanation, please? ,
Dual approach utilizing self microemulsifying technique and novel P-gp inhibitor for effective delivery of taxanes
Authors: Gerrit Borchard
Roop K Khar
Gaurav K Jain
Emmanuelle Sublet
Ajeet K Singh
Farhan J Ahmad
Akash Chaurasiya
Musarrat H Warsi
Journal: Journal of microencapsulation (2012)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: SMEDDS; P-gp inhibitor; taxanes; intestinal epithelium; tumor cells
Affiliations: Faculty of Pharmacy, Hamdard University, New Delhi 110062, India. 

Abstract:  In the present work, concomitant use of self-microemulsifying drug delivery systems (SMEDDS) and a novel third-generation P-gp inhibitor, GF120918 (elacridar), for the effective transport of taxanes (paclitaxel and docetaxel) across an in vitro model of the intestinal epithelium and uptake into tumor cells were investigated. On the basis of solubility studies and ternary phase diagrams, different SMEDDS formulations of taxanes were prepared and characterized. In caco-2 cell permeation study, paclitaxel-loaded SMEDDS along with GF120918 showed a four-fold increase in apparent permeability, while docetaxel-loaded SMEDDS in combination with GF120918 showed a nine-fold increase in permeability, as compared to plain drug solution. Cell uptake studies on A549 cells were performed with microemulsions formed from both SMEDDS formulations loaded with rhodamine 123 dye and showed good uptake than plain dye solution. Confocal laser scanning microscopic images further confirmed the higher uptake of both SMEDDS formulations in the presence of GF120918. 

Retracted: Yes

PubPeer comments:
 Every panel in Figure 7 is identical, after color is changed from green to red, to: Figure 11 of: Ahmad et al., (2018) Preparation and characterization of surface-modified PLGA-polymeric nanoparticles used to target treatment of intestinal cancer, Artificial Cells, Nanomedicine, and Biotechnology, https: doi.org 10.1080 21691401.2017.1324466 ![file] ![file] ,
Disruption of SHH signaling cascade by SBE attenuates lung cancer progression and sensitizes DDP treatment
Authors: Juanjuan Dai
Ning Yu
Yan Wu
Kaikai Gong
Sichuan Xi
Jing Du
Lijuan Yang
Jiwei Guo
Zhen Xie
Jian Zhang
Weiwei Chen
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Sonic Hedgehog pathway; Non-small cell lung cancer; Scutellariabarbata D. Don extraction; SHH signaling pathway; NSCLC progression
Affiliations: Cancer Research Institute, Binzhou Medical University hospital, 256600, Binzhou, P.R. China., Department of Pathology, Binzhou City People's Hospital, 256610, Binzhou, P.R. China., Department of Pathology, Binzhou Medical University Hospital, 256600, Binzhou, P.R. China., Department of Thoracic Surgery, Binzhou Medical University Hospital, 256600, Binzhou, P.R. China., Cancer Research Institute, Binzhou Medical University hospital, 256600, Binzhou, P.R. China. .

Abstract:  Deregulated Sonic Hedgehog (SHH) pathway facilitates the initiation, progression, and metastasis of Non-small cell lung cancer (NSCLC), confers drug resistance and renders a therapeutic interference option to lung cancer patients with poor prognosis. In this study, we screened and evaluated the specificity of a Chinese herb Scutellariabarbata D. Don extraction (SBE) in repressing SHH signaling pathway to block NSCLC progression. Our study confirmed that aberrant activation of the SHH signal pathway conferred more proliferative and invasive phenotypes to human lung cancer cells. This study revealed that SBE specifically repressed SHH signaling pathway to interfere the SHH-mediated NSCLC progression and metastasis via arresting cell cycle progression. We also found that SBE significantly sensitized lung cancer cells to chemotherapeutic agent DDP via repressing SHH components in vitro and in vivo. Mechanistic investigations indicated that SBE transcriptionally and specifically downregulated SMO and consequently attenuated the activities of GLI1 and its downstream targets in SHH signaling pathway, which interacted with cell cycle checkpoint enzymes to arrest cell cycle progression and lead to cellular growth inhibition and migration blockade. Collectively, our results suggest SBE as a novel drug candidate for NSCLC which specifically and sensitively targets SHH signaling pathway. 

Retracted: No

PubPeer comments:
 Another paper with image concerns by this group. Figure 6C appears to have a repeated image, although brightness appears modestly different. *** ![file] , 
 Correction to: Scientific Reports https: doi.org 10.1038 s41598-017-02063-x, published online 15 May 2017 This Article contains errors. In Figure 6C, the image for SBE at 0h (A549 cells) was inadvertently duplicated for Combi at 0 h (A549 cells). The correct Figure 6C appears below as Fig. 1. In Figure 3F, u201cCDK4u201d was mislabelled as u201cCyclin Du201d. The correct Figure 3F appears below as Fig. 2. These changes do not affect the conclusions of the Article. ![file] ,
Chorioallantoic placentation in Galea spixii (Rodentia, Caviomorpha, Caviidae)
Authors: Andrea Mess
Carlos E Ambrósio
Moacir F Oliveira
Maria A Miglino
Phelipe O Favaron
Carlos A G Dantas
Journal: Reproductive Biology and Endocrinology (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Placentation; Guinea pig-related rodents; Animal models; Human placentation; Chorioallantoic placentation
Affiliations: Department of Surgery, Faculty of Veterinary Medicine, University of Sao Paulo, Cidade Universitária, São Paulo, Brazil. 

Abstract:  Background: Placentas of guinea pig-related rodents are appropriate animal models for human placentation because of their striking similarities to those of humans. To optimize the pool of potential models in this context, it is essential to identify the occurrence of characters in close relatives. Methods: In this study we first analyzed chorioallantoic placentation in the prea, Galea spixii, as one of the guinea pig's closest relatives. Material was collected from a breeding group at the University of Mossoró, Brazil, including 18 individuals covering an ontogenetic sequence from initial pregnancy to term. Placentas were investigated by means of histology, electron microscopy, immunohistochemistry (vimentin, alpha-smooth muscle actin, cytokeration) and proliferation activity (PCNA). Results: Placentation in Galea is primarily characterized by an apparent regionalization into labyrinth, trophospongium and subplacenta. It also has associated growing processes with clusters of proliferating trophoblast cells at the placental margin, internally directed projections and a second centre of proliferation in the labyrinth. Finally, the subplacenta, which is temporarily supplied in parallel by the maternal and fetal blood systems, served as the center of origin for trophoblast invasion. Conclusion: Placentation in Galea reveals major parallels to the guinea pig and other caviomorphs with respect to the regionalization of the placenta, the associated growing processes, as well as trophoblast invasion. A principal difference compared to the guinea pig occurred in the blood supply of the subplacenta. Characteristics of the invasion and expanding processes indicate that Galea may serve as an additional animal model that is much smaller than the guinea pig and where the subplacenta partly has access to both maternal and fetal blood systems. 

Retracted: No

PubPeer comments:
 image duplication, recolored ![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. ,
A lentiviral RNAi library for human and mouse genes applied to an arrayed viral high-content screen
Authors: Xiaoping Yang
Gregory Hinkle
Sheila A Stewart
So Young Kim
Brent R Stockwell
Thomas M Eisenhaure
Shi Yin Foo
Anne E Carpenter
Eric S Lander
Jason Moffat
Bruno Piqani
William C Hahn
Nir Hacohen
Angela M Kloepfer
Dorre A Grueneberg
David E Root
David M Sabatini
Jennifer K Grenier
Biao Luo
Journal: Cell (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: lentiviral; shRNA libraries; loss-of-function screens; mammalian cell types; primary cells

Abstract:  To enable arrayed or pooled loss-of-function screens in a wide range of mammalian cell types, including primary and nondividing cells, we are developing lentiviral short hairpin RNA (shRNA) libraries targeting the human and murine genomes. The libraries currently contain 104,000 vectors, targeting each of 22,000 human and mouse genes with multiple sequence-verified constructs. To test the utility of the library for arrayed screens, we developed a screen based on high-content imaging to identify genes required for mitotic progression in human cancer cells and applied it to an arrayed set of 5,000 unique shRNA-expressing lentiviruses that target 1,028 human genes. The screen identified several known and approximately 100 candidate regulators of mitotic progression and proliferation; the availability of multiple shRNAs targeting the same gene facilitated functional validation of putative hits. This work provides a widely applicable resource for loss-of-function screens, as well as a roadmap for its application to biological discovery. 

Retracted: No

PubPeer comments:
 The authors in this paper dealt with the complex intuitionistic fuzzy set, which is a pair of complex numbers within the unit disc with some additional constraints. It is very unusual to use such notions in decision making to evaluate a subject with a given a criterion or attribute. The authors proposed some new aggregation operators, called CIF power averaging operators to aggregate such complex intuitionistic fuzzy sets. However, **such operators, e.g., CIFPA operator in Definition 3.4, are not monotonic. This issue was pointed out in this paper, e.g., Remark 3.1 and Example 3.2.** The authors then used these CIF power averaging operators to handle a multi-criteria decision making problem. However, it is a common practice in decision making of the usual sense **to use an aggregation operator that is order preserving.** Can the authors kindly address this issue? ![file] ![file] ![file] ,