PReD-Bench/PRed-Bench huggingface dataset:
WNT1-inducible signaling protein–1 mediates pulmonary fibrosis in mice and is upregulated in humans with idiopathic pulmonary fibrosis
Authors: Oliver Eickelberg
Andreas Jahn
Ludger Fink
Jochen Wilhelm
Liliana Schaefer
Oana Veronica Amarie
Melanie Königshoff
Nisha Balsara
Frank Rose
Werner Seeger
Monika Kramer
Andreas Günther
Journal: Journal of Clinical Investigation (2009)
Discipline: CLINICAL MEDICINE
Keywords: Idiopathic pulmonary fibrosis; (myo)fibroblast activation; ECM deposition; alveolar epithelial type II cell dysfunction; WNT/beta-catenin signaling pathway
Affiliations: Department of Medicine, University of Giessen Lung Center, Giessen, Germany.

Abstract:  Idiopathic pulmonary fibrosis (IPF) is characterized by distorted lung architecture and loss of respiratory function. Enhanced (myo)fibroblast activation, ECM deposition, and alveolar epithelial type II (ATII) cell dysfunction contribute to IPF pathogenesis. However, the molecular pathways linking ATII cell dysfunction with the development of fibrosis are poorly understood. Here, we demonstrate, in a mouse model of pulmonary fibrosis, increased proliferation and altered expression of components of the WNT/beta-catenin signaling pathway in ATII cells. Further analysis revealed that expression of WNT1-inducible signaling protein-1 (WISP1), which is encoded by a WNT target gene, was increased in ATII cells in both a mouse model of pulmonary fibrosis and patients with IPF. Treatment of mouse primary ATII cells with recombinant WISP1 led to increased proliferation and epithelial-mesenchymal transition (EMT), while treatment of mouse and human lung fibroblasts with recombinant WISP1 enhanced deposition of ECM components. In the mouse model of pulmonary fibrosis, neutralizing mAbs specific for WISP1 reduced the expression of genes characteristic of fibrosis and reversed the expression of genes associated with EMT. More importantly, these changes in gene expression were associated with marked attenuation of lung fibrosis, including decreased collagen deposition and improved lung function and survival. Our study thus identifies WISP1 as a key regulator of ATII cell hyperplasia and plasticity as well as a potential therapeutic target for attenuation of pulmonary fibrosis. 

Retracted: No

PubPeer comments:
 There are overlapping image areas at histology sections from different time points in Fig 3. ![file] This may be some inadvertently mix-up but note that infiltration indeed increases from day 7 to day 14. According to the legend the authors present day 14 experiments Stainings are representative of 2 independent experiments using at least 3 different bleomycin- or saline-treated lung tissues. We can assume that there were 18 animals in each group (Fig 11E) of which =3 animals were eliminated on day 1, 3, 5, 7, 9, 11(Fig S3). In addition up to 50% of the animals in the bleomycin group may have naturally died according to the survival plot (Fig 11E). So it was clearly difficult to present day 14 histology of at least 3 different bleomycin lung tissues. ![file] ,
Ascorbic acid supplementation down-regulates the alcohol induced oxidative stress, hepatic stellate cell activation, cytotoxicity and mRNA levels of selected fibrotic genes in guinea pigs
Authors: P A Abhilash
M Indira
R Harikrishnan
Journal: Free Radical Research (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: oxidative stress; endotoxins; immunological reactions; alcoholic hepatic fibrosis; ascorbic acid
Affiliations: Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, Kerala, India., Department of Biochemistry, University of Kerala,
Kariavattom, Thiruvananthapuram, Kerala, India

Abstract:  Both oxidative stress and endotoxins mediated immunological reactions play a major role in the progression of alcoholic hepatic fibrosis. Ascorbic acid has been reported to reduce alcohol-induced toxicity and ascorbic acid levels are reduced in alcoholics. Hence, we investigated the hepatoprotective action of ascorbic acid in the reversal of alcohol-induced hepatic fibrosis in male guinea pigs (n = 36), and it was compared with the animals abstenting from alcohol treatment. In comparison with the alcohol abstention group, there was a reduction in the activities of toxicity markers and levels of lipid and protein peroxidation products, expression of α-SMA, caspase-3 activity and mRNA levels of CYP2E1, TGF-β(1), TNF-α and α(1)(I) collagen in liver of the ascorbic acid-supplemented group. The ascorbic acid content in liver was significantly reduced in the alcohol-treated guinea pigs. But it was reversed to normal level in the ascorbic acid-supplemented group. The anti-fibrotic action of ascorbic acid in the rapid regression of alcoholic liver fibrosis may be attributed to decrease in the oxidative stress, hepatic stellate cells activation, cytotoxicity and mRNA expression of fibrotic genes CYP2E1, TGF-β(1), TNF-α and α(1) (I) collagen in hepatic tissues. 

Retracted: No

PubPeer comments:
 The same experimental data was used in another publication Redox report: communications in free radical research (2012); pubmed: 22564350 doi: 10.1179 1351000212y.0000000010. Could the authors clarify? ![file] , 
 ![file] ,
Long non-coding RNA KRT19P3 suppresses proliferation and metastasis through COPS7A-mediated NF-κB pathway in gastric cancer
Authors: Ranran Ma
Jie Zheng
Hui Zhang
Haiting Liu
Peng Gao
Journal: Oncogene (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Long non-coding RNAs; lncRNAs; gastric cancer; KRT19P3; downregulation
Affiliations: Key Laboratory for Experimental Teratology of the Ministry of Education and Department of Pathology, School of Medicine, Shandong University, Shandong, P. R. China., Department of Pathology, Weifang Medical University, Shandong, P. R. China., Department of Pathology, Qilu Hospital, Shandong University, Shandong, P. R. China., Key Laboratory for Experimental Teratology of the Ministry of Education and Department of Pathology, School of Medicine, Shandong University, Shandong, P. R. China. ., Department of Pathology, Qilu Hospital, Shandong University, Shandong, P. R. China. .

Abstract:  Long non-coding RNAs (lncRNAs) have emerged as critical regulators in gastric cancer (GC). LncRNA expression microarray data indicate that KRT19P3 (Keratin 19 Pseudogene 3) is downregulated in GC samples. However, the expression pattern and molecular mechanism of KRT19P3 in GC have not been characterized. The present study confirmed the downregulation of KRT19P3 in GC tissues and cells. Decreased expression of KRT19P3 was correlated with larger tumor size, advanced TNM stage, Lauren's classification, positive lymph node metastasis, and poor prognosis. Enforced expression of KRT19P3 significantly inhibited cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, KRT19P3 knockdown had opposite effects. Mechanistically, RNA pull-down and RNA immunoprecipitation assay revealed that KRT19P3 could directly bind COPS7A. KRT19P3 enhanced COPS7A protein stability in GC cells, and KRT19P3 suppressed GC cell proliferation and metastasis partly through regulation of COPS7A expression. COPS7A could promote deubiquitinylation of IκBα, which was executed by CSN-associated deubiquitinylase USP15, and then KRT19P3 inactivated nuclear factor kappa-B (NF-κB) signaling pathway in a COPS7A-dependent manner. For the first time, we revealed that KRT19P3 could suppress tumor growth and metastasis through COPS7A-mediated NF-κB pathway, which may serve as potential targets for treatment of GC in the future. 

Retracted: No

PubPeer comments:
 Should exosomes from different cell lines appear so similar? *** ![file] ,
Requirement for the basic helix-loop-helix transcription factor Dec2 in initial TH2 lineage commitment
Authors: Chen Dong
Xikui Liu
Seon Hee Chang
Juan Peng
Zhiduo Liu
Xuexian O Yang
Bing Sun
Roza Nurieva
Pornpimon Angkasekwinai
Yeonseok Chung
Jinfang Zhu
Journal: Nature Immunology (2009)
Discipline: IMMUNOLOGY
Keywords: CD4(+) T cells; T helper type 2 (T(H)2) lineage; Dec2; basic helix-loop-helix transcription factor; T(H)2 differentiation
Affiliations: Department of Immunology, MD Anderson Cancer Center, Houston, Texas, USA.

Abstract:  How naive CD4(+) T cells commit to the T helper type 2 (T(H)2) lineage is poorly understood. Here we show that the basic helix-loop-helix transcription factor Dec2 was selectively expressed in T(H)2 cells. CD4(+) T cells from Dec2-deficient mice showed defective T(H)2 differentiation in vitro and in vivo in an asthma model and in response to challenge with a parasite antigen. Dec2 promoted expression of interleukin 4 (IL-4), IL-5 and IL-13 during early T(H)2 differentiation and directly bound to and activated transcription of genes encoding the transcription factors JunB and GATA-3. As GATA-3 induces Dec2 expression, our findings also indicate a feed-forward regulatory circuit during T(H)2 differentiation. 

Retracted: No

PubPeer comments:
 In Supplementary Figure 3, the FACS results for WT and DEC2 - - showed identical image while having different percentage labeled, could the authors explain how the percentage where calculated? ![file] , 
 that is ridiculous , 
 In this experiment, we examined whether the transcription factor Dec2 affected B and CD4+ T lymphocyte development. We stained splenocytes of WT and Dec2- - mice with anti-B220 and anti-CD4 antibodies and analyzed the samples using flow cytometry. We found that Dec2-deficiency did not alter the development of B and CD4+ T cells. To illustrate these results, we composed a panel containing flow cytometry plots of each genotype. However, during the composition, we wrongly pasted the WT plot in the position for the Dec2- - sample, which was not noted by the co-authors and the reviewers. The frequencies of each population were manually filled into the figures to assure visibility of numeric characters, according to journalu2019s requirement. We have revisited the original data, and are contacting the journal to correct this unintended error. -Xuexian Yang and Chen Dong ,
Bacterial expression and enzymatic activity analysis of ME1, a ribosome-inactivating protein from Mirabilis expansa
Authors: Ramarao Vepachedu
Sang-Wook Park
Jorge M Vivanco
Neelam Sharma
Journal: Protein expression and purification (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Ribosome-inactivating proteins; RIPs; ME1; Escherichia coli; plant defense
Affiliations: Department of Medicine, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA.

Abstract:  Ribosome-inactivating proteins (RIPs) are toxic proteins synthesized by many plants and some bacteria, that specifically depurinate the 28S RNA and thus interrupt protein translation. RIPs hold broad interest because of their potential use as plant defense factors against pathogens. However, study of the activity of type I RIPs has been hampered since their expression in Escherichia coli has typically been toxic to the model system. Mirabilis expansa, an Andean root crop, produces a type I RIP called ME1 in large quantities in its storage roots. In this study, the cDNA sequence of ME1 was used to successfully express the recombinant ME1 protein in E. coli. The production of recombinant ME1 in E. coli was confirmed by Western blot analysis using anti-ME1 antibodies. The studies with fluorescence-labeled ME1 showed that ME1 can enter bacteria and be distributed in the cytoplasm uniformly, indicating its ability to access the protein synthesis machinery of the bacteria. The recombinant enzyme was active and depurinated yeast ribosomes. However, both native and recombinant ME1 proteins failed to depurinate the E. coli ribosomes, explaining the non-toxicity of recombinant ME1 to E. coli. Structural modeling of ME1 showed that it has folding patterns similar to other RIPs, indicating that ME1 and PAP, which share a similar folding pattern, can show different substrate specificity towards E. coli ribosomes. The results presented here are very significant, as few reports are available in the area of bacterial interaction with type I RIPs. 

Retracted: No

PubPeer comments:
 Figure 1C. * Red and blue boxes: the top half of both the left and middle lane appear to be showing the same area twice. Image contrast adjusted to bring out more details. Could the authors please check if they still have the original blot? ![file] ,
MiR‐202 inhibits cell proliferation, invasion, and migration in breast cancer by targeting ROCK1 gene
Authors: Hui Li
Chengjiu Hu
Fangfang Xu
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: breast cancer; invasion; miR-202; migration; proliferation.
Affiliations: Department of Pathology, Jining No.1 People's Hospital, Jining, China., Department of Oncology, Affiliated Hospital of Jining Medical University, Jining, China.

Abstract:  Purpose: The aim of this study was to research the effect of miR-202 on breast cancer cells proliferation, invasion, and migration. Methods: TCGA analysis was used to research miR-202 expression and overall survival in patients with breast cancer. Transfection with miR-202 mimics or cotransfection with miR-202 mimics and ROCK1 expression vector was performed on breast cancer cells. Reverse transcription polymerase chain reaction was used to detect the miR-202 expression of breast cancer tissues and cells. Western blot was conducted to research the expression of ROCK1, E-cadherin, Twist, N-cadherin, and MMP2. Dual luciferase reporter assay was performed to detect the targeted relationship between ROCK1 and miR-202. MTT and transwell assay were used to detect breast cancer cells proliferation, invasion, and migration. Results: Downregulation of miR-202 was positively correlated with poor prognosis of patients with breast cancer. miR-202 in breast cancer tissues and breast cancer cells was significantly downregulated. Upregulation of miR-202 inhibited the proliferation, migration, and invasion of breast cancer cells. miR-202 promoted E-cadherin expression and inhibited the expression of N-cadherin, Twist, and MMP2. ROCK1 was the target gene of miR-202. miR-202 regulated proliferation, migration, invasion, and expression of related proteins in breast cancer cells by targeting ROCK1 expression. Conclusions: miR-202 inhibited breast cancer cells proliferation, invasion, and migration by targeting the ROCK1 gene. 

Retracted: No

PubPeer comments:
 Large content in this paper (Singhania et al, 2013) has been directly copied from Bhatia et al 2002 Yukti Bhatia, Saroj Mishra V.S. Bisaria (2002) Microbial u03b2-Glucosidases: Cloning, Properties, and Applications, Critical Reviews in Biotechnology, 22:4, 375-407, DOI: 10.1080 07388550290789568 And now I realized that the last author of this paper, Ashok Pandey, is also Editor-in-Chief of the same journal, Bioresource Technology! ![file] ![file] ,
FSC231 alleviates paclitaxel‐induced neuralgia by inhibiting the interactions between PICK1 and GluA2 and activates GSK‐3β and ERK1/2
Authors: Ran Ran
Yuchuan Peng
Jiagao Wang
Yun Xiao
Xi Zhang
Journal: Brain and Behavior (2021)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: FSC231; GSK-3β; GluA2; PICK1; paclitaxel.
Affiliations: Department of Anesthesiology Renmin Hospital Hubei University of Medicine  Shiyan P. R. China

Abstract:  Background: FSC231, a PSD-95/DLG/ZO-1 (PDZ) domain inhibitor of protein kinase Cα interacting protein 1 (PICK1), has analgesic effects, but the mechanism remains unclear. Methods: The expression level of PICK1 in dorsal root ganglion (DRG) of rats was changed by vector plasmid, and the effect of PICK1 on paclitaxel (PTL)-induced neuralgia of rats was observed in collaboration with FSC231 treatment. The possible molecular mechanisms were explored by quantitative real-time polymerase chain reaction (qRT-PCR), Western Blot and co-immunoprecipitation (Co-IP) techniques. Results: PTL treatment can significantly reduce mechanical withdrawal threshold (MWT), shorten thermal withdrawal latency (TWL), promote DRG inflammation and release of substance P (SP), stimulate PICK1 expression, decrease α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor 2 (AMPAR, GluA2) level and increase glycogen synthase kinase-3β (GSK-3β) and extracellular regulated protein kinases1/2 (ERK1/2) phosphorylation in rats, while FSC231 treatment can alleviate the above effects induced by PTL. Overexpression of PICK1 can counteract reduced PICK1 level, increased GluA2 level and decreased GSK-3β and ERK1/2 phosphorylation levels caused by FSC231 treatment. The results of Co-IP confirmed the interactions between PICK1 and GluA2. Both FSC231 treatment and silent PICK1 improved PTL-induced MWT reduction, TWL shortening, inflammation, SP release and related gene expression changes, with cumulative effect. Conclusion: FSC231 activates GSK-3β/ERK1/2 by inhibiting the interaction between PICK1 and GluA2 and alleviates PTL-induced DRG neuralgia in rats. 

Retracted: No

PubPeer comments:
 The subject animals were too light to be rats. Perhaps, mice? Also, $8 cdot 10 = 80  eq 40$. ![file] ![file] ,
PinX1 regulation of telomerase activity and apoptosis in nasopharyngeal carcinoma cells
Authors: Yu-Hong Qian
Jun-Qi Wang
Chao-Sheng Yu
Cong-Xiang Shen
Ping-Neng Zhong
Hai-Li Wang
Zhong Wen
Xiao-Fen Lai
Journal: Journal of Experimental & Clinical Cancer Research (2012)
Discipline: CLINICAL MEDICINE
Keywords: PinX1; telomerase inhibitor; tumor suppressor gene; nasopharyngeal carcinoma; hTERT
Affiliations: Department of Otolaryngology Head and Neck Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.

Abstract:  Background: Human interacting protein X1 (PinX1) has been identified as a critical telomerase inhibitor and proposed to be a putative tumor suppressor gene. Loss of PinX1 has been found in a large variety of malignancies, however, its function in inhibiting telomerase activity of tumor cells is not well documented. Here we show that PinX1 is essential for down-regulation telomerase activity of nasopharyngeal carcinoma. Methods: Expression vectors of human PinX1 (pEGFP-C3-PinX1) and its small interfering RNA (PinX1-FAM-siRNA) were constructed and transfected into NPC. Their effects on mRNA of telomerase catalytic subunit (hTERT), telomerase activity, cell proliferation, cell migration, wound healing, cell cycles and apoptosis were examined using semi-quantitative RT-PCR, stretch PCR, MTT assay, Transwell, scratch assay and flow cytometry, respectively. Results: Transfection of pEGFP-C3-PinX1 and PinX1-FAM-siRNA increased and reduced PinX1 mRNA by 1.6-fold and 70%, respectively. Over-expression of PinX1 decreased hTERT mRNA by 21%, reduced telomerase activity, inhibited cell growth, migration and wound healing ability, arrested cells in G0/G1 phase, and increased apoptotic index. In contrast, down-regulation of PinX1 did not alter the above characteristics. Conclusions: PinX1 may play important roles in NPC proliferation, migration and apoptosis and has application potential in tumor-targeted gene therapy. 

Retracted: No

PubPeer comments:
 unexpected image duplication ![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. , 
 Overlap was detected in Fig. 6 ![file] , 
 I m very sorry to reply you now, because I just learned this information.u00a0u00a0u00a0u00a0u00a0u00a0u00a0u00a0u00a0u00a0u00a0 First of all, thank you very much for your attention. Secondly, the experiment was completed more than 10 years ago. Due to the age and computer failure, some original experimental data have been lost, but I carefully recalled the experiment at that time. The similarity here may be the misuse of pictures, but it is indeed the experimental result repeated many times, which does not affect the correctness of the experimental result. ,
A self-aggregating peptide: implications for the development of thermostable vaccine candidates
Authors: Alicia Sampieri
J Iván Sánchez-Betancourt
Adolfo Cruz-Reséndiz
Luis Vaca
Carlos Bastián-Eugenio
Jesús Zepeda-Cervantes
Goar Gevorkian
Gonzalo Acero
Journal: BMC biotechnology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Immunology; Particles; Self-assembling; Thermostable; Vaccines.
Affiliations: Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, CDMX 04510, Mexico City, Mexico., Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, CDMX 04510, Mexico City, Mexico., Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, CDMX 04510, Mexico City, Mexico., Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, CDMX 04510, Mexico City, Mexico. ., Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA, 98124, USA. .

Abstract:  Background: The use of biomaterials has been expanded to improve the characteristics of vaccines. Recently we have identified that the peptide PH(1-110) from polyhedrin self-aggregates and incorporates foreign proteins to form particles. We have proposed that this peptide can be used as an antigen carrying system for vaccines. However, the immune response generated by the antigen fused to the peptide has not been fully characterized. In addition, the adjuvant effect and thermostability of the particles has not been evaluated. Results: In the present study we demonstrate the use of a system developed to generate nano and microparticles carrying as a fusion protein peptides or proteins of interest to be used as vaccines. These particles are purified easily by centrifugation. Immunization of animals with the particles in the absence of adjuvant result in a robust and long-lasting immune response. Proteins contained inside the particles are maintained for over 1 year at ambient temperature, preserving their immunological properties. Conclusion: The rapid and efficient production of the particles in addition to the robust immune response they generate position this system as an excellent method for the rapid response against emerging diseases. The thermostability conferred by the particle system facilitates the distribution of the vaccines in developing countries or areas with no electricity. 

Retracted: No

PubPeer comments:
 Figure 3C. * Red boxes: Two panels appear to show an overlap. ![file] ,
FGF1–FGFR1 axis promotes tongue squamous cell carcinoma (TSCC) metastasis through epithelial–mesenchymal transition (EMT)
Authors: Yancan Liang
Jiuyang Jiao
Xiaopeng Zhao
Dongxiao Tang
Chaobin Pan
Journal: Biochemical and Biophysical Research Communications (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Epithelial mesenchymal-transition; FGF1–FGFR1 axis; Tongue squamous cell carcinoma; Tumor metastasis.
Affiliations: Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China; Department of Oral & Maxillofacial Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China., Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China; Department of Oral & Maxillofacial Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China. Electronic address: .

Abstract:  Increasing evidences suggest a close association between tumor metastasis and the inflammatory factors secreted by tumor microenvironment. It has been reported that epithelial mesenchymal-transition (EMT) plays a significant role during multiple types of tumor metastasis and progression induced by inflammatory factor from tumor microenvironment. Previous researches implied that fibroblast growth factor 1 (FGF1) can promote tumor progression and cause poor prognosis in several types of malignant tumors via interacting with its receptor fibroblast growth factor receptor 1 (FGFR1). However, the effects of FGF1-FGFR1 on tongue squamous cell carcinoma (TSCC) are not yet completely understood. In the present study, we evaluated the effects and function of FGF1-FGFR1 axis on TSCC metastasis. In addition, we investigated whether the EMT pathway is involved in these effects, thus modulating the TSCC progression. The expression of FGFR1 was measured both in tongue cancer cell lines and tissues by qRT-PCR and western blot. We found that FGFR1 was up-regulated in TSCC tissues compared to non-neoplastic tongue tissues. Additionally, overexpression of FGFR1 is positively associated with poor differentiation and metastasis potential. Furthermore, the function of FGF1-FGFR1 was examined in TSCC cell line. The results implied that FGF1 can obviously promote Cal27 cells migration and invasion abilities through FGFR1, while the motile and invasive capabilities can be severely attenuated when knockdown the expression of FGFR1 by specific siRNAs. Further investigation results show that FGF1-FGFR1 axis promotes TSCC metastasis by modulating EMT pathway. However, this effect can be inhibited by blocking the FGF1-FGFR1 axis using FGFR1 specific siRNAs. In conclusion, our findings of the present study provide the evidences that FGF1-FGFR1 axis promotes the TSCC metastasis through the EMT pathway. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have overlapping images ![file] ,
Nuclear Spin Attenuates the Anesthetic Potency of Xenon Isotopes in Mice
Authors: Lei Yang
Younian Xu
Lisha Fu
Yatisha Chummum
Shihai Zhang
Hui Liu
Na Li
Huan Tao
Dongshi Lu
Chenchen Wang
Journal: Anesthesiology (2018)
Discipline: CLINICAL MEDICINE
Keywords: Xenon; isotopes; nuclear spin; anesthetic potency; mice

Abstract:  What we already know about this topic: WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Xenon is an elemental anesthetic with nine stable isotopes. Nuclear spin is a quantum property which may differ among isotopes. Xenon 131 (Xe) has nuclear spin of 3/2, xenon 129 (Xe) a nuclear spin of 1/2, and the other seven isotopes have no nuclear spin. This study was aimed to explore the effect of nuclear spin on xenon anesthetic potency. Methods: Eighty C57BL/6 male mice (7 weeks old) were randomly divided into four groups, xenon 132 (Xe), xenon 134 (Xe), Xe, and Xe groups. Due to xenon's low potency, loss of righting reflex ED50 for mice to xenon was determined with 0.50% isoflurane. Loss of righting reflex ED50 of isoflurane was also measured, and the loss of righting reflex ED50 values of the four xenon isotopes were then calculated. The exact polarizabilities of the isotopes were calculated. Results: Combined with 0.50% isoflurane, the loss of righting reflex ED50 values were 15 ± 4%, 16 ± 5%, 22 ± 5%, and 23 ± 7% for Xe, Xe, Xe, and Xe, respectively. For xenon alone, the loss of righting reflex ED50 values of Xe, Xe, Xe, and Xe were 70 ± 4%, 72 ± 5%, 99 ± 5%, and 105 ± 7%, respectively. Four isotopes had a same exact polarizability of 3.60 Å. Conclusions: Xenon isotopes with nuclear spin are less potent than those without, and polarizability cannot account for the difference. The lower anesthetic potency of Xe may be the result of it participating in conscious processing and therefore partially antagonizing its own anesthetic potency. Nuclear spin is a quantum property, and our results are consistent with theories that implicate quantum mechanisms in consciousness. 

Retracted: No

PubPeer comments:
 The authors describe evidence that different isotopes of Xenon have different potencies. They then purport to show that this cannot be due to differences in polarizability. To do this they calculate polarizabilities using the Density Functional Theory (DFT) code Gaussian, one assumes by putting a different isotope mass in the atom properties. They find no difference in the polarizabilities and conclude that the different potencies must be due to spin. The problem is that electronic structure differences caused by a different number of neutrons in the nucleus cannot be calculated by a DFT code, which assumes nuclei are point charges. The conclusion of the paper is therefore unwarranted. ,
Maternal isolation alters the expression of neural proteins during development: ‘Stroking’ stimulation reverses these effects
Authors: Cynthia B de Medeiros
Diptendu Chatterjee
Alison S Fleming
Munmun Chatterjee-Chakraborty
Jonathan Cauchi
Stephanie Rees
Journal: Brain Research (2007)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Rat pups; 'pup-in-a-cup' regime; Institutional Inattention/Overactivity Syndrome; brain proteins; Neu-N
Affiliations: University of Toronto at Mississauga, 3359 Mississauga Rd N, Mississauga, Ontario, Canada L5L 1C6.

Abstract:  Rat pups reared apart from their siblings, mother, and nest environment in the 'pup-in-a-cup' regime show many alterations in behavior reminiscent of the Institutional Inattention/Overactivity Syndrome that characterizes children whose first few months are spent in institutions. In this report, we compare mother-reared (MR) and artificially reared (AR) male rats in concentrations and distributions of brain proteins that are involved in normal brain development. When assessed during the juvenile period and in adulthood, AR animals showed elevations in Neu-N (a neuronal marker) and in S-100 (an astrocyte marker) but reductions in synaptophysin (synapse protein), N-CAM (cell-adhesion molecule), GAP-43 (axon elongation protein), and BDNF (brain derived neurotrophic factor) in comparison to MR controls in many brain sites involved in attention, impulsivity, activity, and social behavior. Daily 'licking-like' stimulation provided to AR animals (AR-MAX) throughout early development that reverses many of the behavioral deficits, also reverses many of the isolation effects on brain proteins. Study 2 showed that elevations in the number of neurons in combination with decreases in functionality are associated with a reduction in neuronal pruning and apoptosis during the very early post-partum period in AR animals and their reversal through daily 'licking-like' stimulation. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: In the S-100 column the AMYG and NA panels look more similar than expected, but with a different aspect ratio. Note a small dot above the left-most lane, and another small dot at the top of the band in the right-most lane. ![file] , 
 Figure 5. * Blue boxes: In the NCAM (p180) column, the mPFC and NA panels look more similar than expected, but cut out slightly differently. Note a slanted strip under the 3rd lane from the left. ![file] ,
Catalase ameliorates diabetes-induced cardiac injury through reduced p65/RelA- mediated transcription of BECN1
Authors: Gen Chen
Yang Wang
Xu Wang
Xiaozhong Huang
Kungao Zhan
Yangzhi Liang
Youli Tao
Weitao Cong
Mei Xue
Yewei Huang
Ruijie Chen
Santie Li
Dandan Ruan
Lingchun Lv
Zhiwei Chen
Litai Jin
Jianjun Lin
Ying Wang
Journal: Journal of Cellular and Molecular Medicine (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Autophagy; Cardiomyopathy; Catalase; Diabetes; NF-κB.
Affiliations: School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, China., The Ningbo Medical Centre Li Huili Hospital, Ningbo, China., The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., The Health Examination Center, the 117th Hospital of Chinese People's Liberation Army, Hangzhou, China., The Affiliated Xiangshan Hospital of Wenzhou Medical University, Ningbo, Zhejiang, China., The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui, China., Department of Histology and Embryology, Institute of Neuroscience, Wenzhou Medical University, Wenzhou, China.

Abstract:  Catalase is an antioxidative enzyme that converts hydrogen peroxide (H2 O2 ) produced by superoxide dismutase from highly reactive superoxide (O2- ) to water and oxygen molecules. Although recent findings demonstrate that catalase, autophagy and the nuclear factor κB (NF-κB) signalling pathway are centrally involved in diabetic cardiomyopathy (DCM), the interplay between the three has not been fully characterized. Thus, the mechanism responsible for catalase-mediated protection against heart injury in diabetic mice was investigated in this study, as well as the role of NF-κB-p65 in the regulation of autophagic flux was investigated in this study. Western blot analysis revealed that catalase inhibited NF-κB activity and decreased LC3-II (microtubule-associated protein 1 light chain 3) and beclin-1 (Atg6) expression. Furthermore, up-regulation of autophagy was detrimental for cardiac function in diabetic mice. Catalase overexpression reduced the level of NF-κB subunit in the nucleus, where it initiates autophagy through activation of the key autophagy gene BECN1. To evaluate the role of the NF-κB pathway in diabetes-induced autophagy, Bay11-7082, an NF-κB inhibitor, was injected into diabetic mice, which suppressed NF-κB and attenuated diabetes-induced autophagy and myocardial apoptosis. In agreement with the in vivo results, Bay11-7082 also inhibited high-glucose-induced activation of NF-κB and the up-regulation of LC3-II and beclin-1 expression in H9c2 cells. In addition, high-glucose-induced activation of autophagic flux and apoptosis were largely attenuated by p65 siRNA, suggesting that catalase ameliorates diabetes-induced autophagy, at least in part by increasing the activity of the NF-κB pathway and p65-mediated transcription of BECN1. 

Retracted: No

PubPeer comments:
 Fig 2 ![file] Fig 3 ![file] Unexpected similarities in Gapdh of Fig 2C and Fig 3A. , 
 Judging from the MWs of the bands in the Figs, they most likely come from different membranes. Any full-length blots? ,
Telomere damage induced by the G-quadruplex ligand RHPS4 has an antitumor effect
Authors: Eric Gilson
Giovanna Chiorino
Rossella Galati
Maurizio D&#x27;Incalci
Malcolm F G Stevens
Béatrice Horard
Serge Bauwens
Marcella Mottolese
Isabella Sperduti
Maria Blasco
Angela Rizzo
Carlo Leonetti
Marco Scarsella
Annamaria Biroccio
Erica Salvati
Antonella Stoppacciaro
Gabriella Zupi
Journal: Journal of Clinical Investigation (2007)
Discipline: CLINICAL MEDICINE
Keywords: Telomeres; G-quadruplex; RHPS4; DNA damage response; Telomeric foci
Affiliations: Experimental Chemotherapy Laboratory, Regina Elena Cancer Institute, Rome, Italy.

Abstract:  Functional telomeres are required for the replicability of cancer cells. The G-rich strand of telomeric DNA can fold into a 4-stranded structure known as the G-quadruplex (G4), whose stabilization alters telomere function limiting cancer cell growth. Therefore, the G4 ligand RHPS4 may possess antitumor activity. Here, we show that RHPS4 triggers a rapid and potent DNA damage response at telomeres in human transformed fibroblasts and melanoma cells, characterized by the formation of several telomeric foci containing phosphorylated DNA damage response factors gamma-H2AX, RAD17, and 53BP1. This was dependent on DNA repair enzyme ATR, correlated with delocalization of the protective telomeric DNA-binding protein POT1, and was antagonized by overexpression of POT1 or TRF2. In mice, RHPS4 exerted its antitumor effect on xenografts of human tumor cells of different histotype by telomere injury and tumor cell apoptosis. Tumor inhibition was accompanied by a strong DNA damage response, and tumors overexpressing POT1 or TRF2 were resistant to RHPS4 treatment. These data provide evidence that RHPS4 is a telomere damage inducer and that telomere disruption selectively triggered in malignant cells results in a high therapeutic index in mice. They also define a functional link between telomere damage and antitumor activity and reveal the key role of telomere-protective factors TRF2 and POT1 in response to this anti-telomere strategy. 

Retracted: No

PubPeer comments:
 There appears to be image overlap between figure 6H and images in Figure 7, as well as within Figure 7. See also: https: pubpeer.com search?q=authors%3A%22Rossella+galati%22 *** 6H ![file] Figure 7 ![file] *** ![file] ,
Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205
Authors: Jian-Wei Zhang
Fei Wang
Xi-Gang Kang
Feng Liang
Li Wang
Hong-Yan Zhang
Journal: Cancer Chemotherapy and Pharmacology (2017)
Discipline: CLINICAL MEDICINE
Keywords: Breast cancer; Long noncoding RNA-ROR; MicroRNA-205; Tamoxifen resistance.
Affiliations: Oncology Department, PLA Army General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, People's Republic of China. ., General Surgery Department, Affiliated Hospital of Academic of Military Medical Science, Beijing, 100071, People's Republic of China., Oncology Department, PLA Army General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, People's Republic of China.

Abstract:  Purpose: To explore how long noncoding RNA-ROR (lncRNA-ROR) affects the tamoxifen resistance of breast cancer cells. Methods: Breast epithelial (MCF10A), breast cancer (MCF7), and natural tamoxifen-resistant breast cancer (MDA-MB-231) cell lines were selected, and the relative lncRNA-ROR expressions were detected using quantitative real-time polymerase chain reaction (qRT-PCR). In vitro induction of TR5 cell line was performed. There were six groups: MCF7, MCF7/TR5, MDA-MB-231, MCF7-ROR, MCF7/TR5 ROR-siRNA, and the MDA-MB-231 ROR-siRNA groups. CCK-8 assay was conducted to assess the changes in drug resistance of each group. The expression of the epithelial mesenchymal transition (EMT) marker was detected using Western blotting. Transwell was selected to test the invasive ability of the cells. Expressions of microRNA-205 (miR-205) and ZEB1/2 were detected using qRT-PCR . Results: Compared with the MCF7 cells, the proliferation rates of the MCF7/TR5 and MDA-MB-231 cells were significantly increased. Compared with the MCF7 cells, the MCF7-ROR cells had remarkably higher proliferation rates, down-regulated E-cadherin and miR-205 expressions, as well as increased vimentin, invasive ability, and mRNA expression of ZEB1 and ZEB2. Compared with the MCF7/TR5 and MDA-MB-231 cells, up-regulated E-cadherin and miR-205 expression, down-regulated expression of vimentin, ZEB1, and ZEB2 mRNA, and decreased invasive ability were observed in the MCF7/TR5 ROR-siRNA and MDA-MB-231 ROR-siRNA cells. Conclusion: In MDA-MB-231 cells, down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2. 

Retracted: No

PubPeer comments:
 Fig. 6  Effects of interfered or overexpressed long noncoding RNA-ROR on the invasion of breast cancer cells . ![file] Conceivably linked in some way to Figure 13A from [Lu et al (2018)] .  Transwell results (A, u00d7 200) ... in each group . ![file] UPDATE: Another sighting! Fig Fig. 4A,B from [Bai et al (2016)] .  Comparisons of migratory and invasive cell numbers among the blank, NC, p16INK4A and p14ARF groups. ... A Transwell migration of cells in each groups; B Transwell invasion of cells in each groups . ![] UPDATE #2. Fig 5 from [Zhou et al (2016)] . ![] ,
G protein-coupled receptor 56 regulates matrix production and motility of lung fibroblasts
Authors: Huaping Dai
Dong Leng
Chen Wang
Dianhua Jiang
Zhanyong Wang
Jun Wang
Jiurong Liang
Jian Yang
Journal: Experimental Biology and Medicine (2014)
Discipline: CLINICAL MEDICINE
Keywords: Idiopathic pulmonary fibrosis; G protein-coupled receptor 56 (GPR56); fibrogenesis; fibroblasts; fibronectin
Affiliations: Department of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing Institute of Respiratory Medicine, Beijing 100020, China, Clinical Laboratory, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China, Laboratory Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China, Faculty of Respirology, Capital Medical University, Beijing 100069, China, Department of Physiology, Capital Medical University, Beijing 100069, China, Cedars-Sinai Medical Center Department of Medicine, Los Angeles, CA 90048, USA

Abstract:  Idiopathic pulmonary fibrosis is a chronic, progressive, and fatal fibrotic lung disease with a poor prognosis, but no effective treatment is available. G protein-coupled receptor 56 (GPR56) plays a role in cell adhesion and tumor progression, but its function in fibrogenesis has not been explored. In this in vitro study, we found that GPR56 in IPF fibroblasts was lower than in normal fibroblasts. GPR56 regulated the production of fibronectin and type I collagen, and also changed the migratory and invasive capacity of lung fibroblasts. However, it was not sufficient to activate some classic markers of fibroblast and myofibroblast, such as α-smooth muscle actin and fibroblast specific protein 1. These findings demonstrate that reduced expression of GPR56 in lung fibroblasts may be an important link with pulmonary fibrosis, playing a role in regulating some important fibroblast functions. 

Retracted: No

PubPeer comments:
 ![file] , 
 This response is on behalf of first author, Jian Yang. We thank the reader noting that Figure 3a and Figure 6c contained the similar u03b2-actin images. Indeed, they are the same image. Figure 3a shows fibronectin and collagen I expressions of MRC-5 interfered by GPR56 siRNA were significantly increased. Figure 6c shows MMP-9 expression of MRC-5 interfered by GPR56 siRNA was significantly increased. Both Figure 3a and Figure 6c were from the same samples and same treatments. When the figures were ensembled for publication, the data were separated into two panels, 3a showing siRNA effect on matrix production, while 6c showing mechanistically MMP-9 increase, and the same u03b2-actin image was used. We regret the error. If you have any further concerns, please contact the first author directly through his email, Jian Yang kongji_1984@bzmc.edu.cn . , 
 Then why the GPR56 blots in both figures are not the same? ,
Circulating MicroRNAs as Novel Potential Biomarkers for Left Ventricular Remodeling in Postinfarction Heart Failure
Authors: Ping Yang
Guangyuan Gao
Miao Liu
Weiwei Chen
Xu Yan
Journal: Disease markers (2019)
Discipline: CLINICAL MEDICINE
Keywords: circulating microRNAs; left ventricular remodeling; postinfarction heart failure; myocardial infarction; plasma miRNAs
Affiliations: Department of Cardiology, China-Japan Union Hospital of Jilin University, Changchun 130031, China., Jilin Provincial Molecular Biology Research Center for Precision Medicine of Major Cardiovascular Disease, Changchun 130031, China.

Abstract:  Circulating microRNAs (miRNAs) have been proposed as potential biomarkers for left ventricular remodeling in postinfarction heart failure (HF). However, the diagnostic reproducibility of the use of circulating miRNAs may be affected by the temporal expression of miRNAs following myocardial infarction (MI). In the current study, using a MI-induced HF rat cohort (4-, 8-, and 12-week post-MI groups), we investigated the temporal expression of plasma miRNAs during the development of left ventricular remodeling. The plasma miRNA expression profile was obtained using miRNA sequencing. The expression of candidate miRNAs in plasma and tissues was examined with real-time PCR. Target genes of candidate miRNAs were predicted using a parallel miRNA-messenger RNA expression profiling approach. The value of plasma miRNAs as biomarkers for left ventricular remodeling was evaluated in patients with postinfarction HF (n = 32) and control patients with stable angina and without significant coronary lesions and HF (n = 16) with real-time PCR. Although the expression levels of miR-20a-5p, miR-340-5p, and let-7i-5p were temporally regulated in plasma, myocardium, and peripheral blood mononuclear cells, the expression levels of plasma miRNAs, especially miR-20a-5p, were associated with the development of left ventricular remodeling in the postinfarction HF rat cohort. The target genes of these 3 miRNAs were associated with the mechanistic target of rapamycin, nuclear factor-κB, tumour necrosis factor, apoptosis, and p53 signaling pathways. Additionally, the plasma levels of miR-20a-5p, miR-340-5p, and let-7i-5p were significantly increased in patients with postinfarction HF. However, only the expression levels of miR-20a-5p presented significant positive correlations with left ventricular internal end diastolic dimension and left ventricular end diastolic volume. In conclusion, the expression levels of plasma miR-20a-5p were significantly associated with the degree of left ventricular dilatation, and plasma miR-20a-5p may be a potential biomarker for postinfarction left ventricular remodeling. 

Retracted: No

PubPeer comments:
 Different microRNAs got similar data and different AUC. ![file] ,
Intraplastidial trafficking of a phage-type RNA polymerase is mediated by a thylakoid RING-H2 protein
Authors: Jacinthe Azevedo
Laurence Maréchal-Drouard
Thierry Lagrange
Mohamed-Ali Hakimi
Florence Courtois
Silva Lerbs-Mache
Emilie Demarsy
Jean-Pierre Alcaraz
Pankaj Jaiswal
Journal: Proceedings of the National Academy of Sciences of the United States of America (2008)
Discipline: Multidisciplinary
Keywords: Plastid genome; RNA polymerases; RPOTp; RPOTmp; chloroplast transcription
Affiliations: Laboratoire Plastes et Differénciation Cellulaire, Université Joseph Fourier and Centre National de la Recherche Scientifique, B.P. 53, F-38041 Grenoble Cedex 9, France.

Abstract:  The plastid genome of dicotyledonous plants is transcribed by three different RNA polymerases; an eubacterial-type enzyme, PEP; and two phage-type enzymes, RPOTp and RPOTmp. RPOTp plays an important role in chloroplast transcription, biogenesis, and mesophyll cell proliferation. RPOTmp fulfills a specific function in the transcription of the rrn operon in proplasts/amyloplasts during seed imbibition/germination and a more general function in chloroplasts during later developmental stages. In chloroplasts, RPOTmp is tightly associated with thylakoid membranes indicating that functional switching of RPOTmp is connected to thylakoid association. By using the yeast two-hybrid system, we have identified two proteins that interact with RPOTmp. The two proteins are very similar, both characterized by three N-terminal transmembrane domains and a C-terminal RING domain. We show that at least one of these proteins is an intrinsic thylakoid membrane protein that fixes RPOTmp on the stromal side of the thylakoid membrane, probably via the RING domain. A model is presented in which light by triggering the synthesis of the RING protein determines membrane association and functional switching of RPOTmp. 

Retracted: No

PubPeer comments:
 Tumor are surprisingly similar although they should be treated differently. ![file] , 
 In addition to the duplication in Fig 3D noted above, there is another duplication in Fig 3E: ![file] Further, while reading some of the authors other publications, I noticed an alarming similarity between Table 1 in Miao et al. and Table 1 of [Ren et al. (2014) IUBMB Life] , on which Yongfu Zhao is last author. These tables are meant to describe distinct patient populations with different cancers, yet the data look strikingly similar. ![file] ![file] ,