PReD-Bench/PRed-Bench huggingface dataset:
<p>The lncRNA HOXA11-AS regulates Rab3D expression by sponging miR-125a-5p promoting metastasis of osteosarcoma</p>
Authors: Yueyang Fang
Yong Hu
Hao Wang
Kun Cao
Li Guo
Zheng Jiang
Journal: Cancer Management and Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: HOXA11-AS; Rab3D; long non-coding RNAs (lncRNAs); miR-125a-5p; osteosarcoma (OS).
Affiliations: Department of Orthopaedics, The First Hospital Of Anhui Medical University, Hefei, People's Republic of China., Department of Orthopaedics, The Second Hospital Of Shanxi Medical University, Taiyuan, People's Republic of China.

Abstract:  Objective: Many studies have shown that long non-coding RNAs (lncRNAs) are closely related to various cancers. This study aims to explore the roles of lncRNA HOXA11-AS in the development and progression of osteosarcoma (OS). Methods: The expression levels of HOXA11-AS and miR-125a-5p in tumor tissues and the adjacent tissues were detected by RT-PCR method. The proliferation, migration and invasion of MG-63 and KHOS cells were determined. Results: It was found that HOXA11-AS expression levels in OS tissues and OS cell lines were higher than those in OS adjacent tissues and normal human osteoblast cell lines. The higher expression level of HOXA11-AS was positively correlated with more severe clinical stage, distant metastasis and poor prognosis of OS. Inhibition of HOXA11-AS expression could reduce metastasis and invasion of OS cell lines. In addition, HOXA11-AS was found to be an endogenous inhibitor of miR-125a-5p, it down regulated the expression level of miR-125a-5p, and this process could promote the expression of Rab3D, the target gene of miR-125a-5p. Conclusion: Our study elucidated the role of a new HOXA11-AS/miR-125a-5p/Rab3D regulatory pathway in promoting OS metastasis. 

Retracted: No

PubPeer comments:
 Unexpected similar in Figure 3B. You many find more in this article.  , 
 Between Fig 3B and Fig. 5C, there s a reused image with 180 deg rotation  ,
Cytokine and adhesion molecule expression in human monocytes and endothelial cells stimulated with bacterial heat shock proteins
Authors: M Galdiero
A Marcatili
G C de l&#x27;Ero
Journal: Infection and Immunity (1997)
Discipline: IMMUNOLOGY
Keywords: Bacterial heat shock proteins; interleukin-6; tumor necrosis factor alpha; granulocyte-monocyte colony-stimulating factor; monocytes
Affiliations: Dipartimento di Patologia, Facolt√† di Veterinaria, Universit√† degli Studi di Napoli Federico II, Naples, Italy.

Abstract:  Bacterial heat shock proteins (HSPs) from Escherichia coli (GroES, GroEL, and DNAk) were tested for their ability to induce by themselves the expression and release of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and granulocyte-monocyte colony-stimulating factor (GM-CSF) by human monocytes and GM-CSF, IL-6, E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by human umbilical vein endothelial cells (HUVEC). Our study demonstrated that treatment of monocytes with DNAk increased IL-6, TNF-alpha, and GM-CSF release in a dose-dependent manner. The same effect was elicited by GroEL but at a lower rate. Treatment of HUVEC cultures with DNAk and GroEL also increased GM-CSF, IL-6, E-selectin, ICAM-1, and VCAM-1 release in a dose-dependent fashion. In any case, the greatest release was obtained by using DNAk and GroEL at a concentration of 1 microg/ml. DNAk and GroEL were also able to up-regulate the surface expression of E-selectin, ICAM-1, and VCAM-1. As detected by reverse transcription-PCR analysis, DNAk and GroEL also increased the steady-state levels of cytokines and adhesion molecules in human monocytes and endothelial cells. In our study GroES showed a significant activity only on the release, surface expression, and mRNA transcription of E-selectin. Adhesion molecule expression seems to be a direct effect of HSPs and not via cytokines. Furthermore, these effects are due to HSPs properties because they are inhibited by specific monoclonal antibodies. These findings support the potential role of HSPs in modulating cell interactions during immunological and inflammatory responses. 

Retracted: No

PubPeer comments:
 Figure 5 (human monocytes) and Figure 6 (human endothelial cells): * Pink boxes: The b-actin panels appear to look identical.  ,
Hypoglycemic and antioxidant effects of leaf essential oil of Pelargonium graveolens L‚ÄôH√©r. in alloxan induced diabetic rats
Authors: Sami Sayadi
Hedya Jemai
Mohamed Bouaziz
Abdelfattah El Feki
Ines Feki
Maher Boukhris
Journal: Lipids in Health and Disease (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Rose-scented geranium; Pelargonium graveolens; hypoglycemic; antioxidative activities; essential oil
Affiliations: Laboratoire des Bioproc√©d√©s Environnementaux, Centre de Biotechnologie de Sfax, Universit√© de Sfax, BP: 1177, 3018 Sfax, Tunisia.

Abstract:  Background: Rose-scented geranium (Pelargonium graveolens L'H√©r.), which is used in traditional Tunisian folk medicine for the treatment of hyperglycaemia, is widely known as one of the medicinal herbs with the highest antioxidant activity. The present paper is conducted to test the hypoglycemic and antioxidative activities of the leaf essential oil of P. graveolens. Methods: The essential oil P. graveolens was administered daily and orally to the rats at two doses of 75 mg/kg and 150 mg/kg body weight (b.w.) for 30 days. The chemical composition of P. graveolens essential oil, body weight, serum glucose, hepatic glycogen, thiobarbituric acid-reactive substances (TBARS), the components of hepatic, and renal and serum antioxidant systems were evaluated. The hypoglycemic effect of rose-scented geranium was compared to that of the known anti-diabetic drug glibenclamide (600 Œºg/kg b.w.). Results: After the administration of two doses of essential oil of Pelargonium graveolens L'H√©r. together with glibenclamide which is known by its antidiabetic activities and used as reference (600 Œºg/kg b.w.), for four weeks, the serum glucose significantly decreased and antioxidant perturbations were restored. The hypoglycemic effect of P. graveolens at the dose of 150 mg/kg b.w. was significantly (p &lt; 0.05) more effective than that of glibenclamide. It is through the histological findings in hepatic and renal tissues of diabetic rats that these beneficial effects of geranium oils were confirmed. Conclusions: It suggests that administration of essential oil of P. graveolens may be helpful in the prevention of diabetic complications associated with oxidative stress. Our results, therefore, suggest that the rose-scented geranium could be used as a safe alternative antihyperglycemic drug for diabetic patients. 

Retracted: No

PubPeer comments:
 image duplication  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. ,
JCDB: a comprehensive knowledge base for Jatropha curcas, an emerging model for woody energy plants
Authors: Zeng-Fu Xu
Wen Chen
Xuan Zhang
Changning Liu
Jing Li
Maosheng Chen
Bang-Zhen Pan
Journal: BMC genomics (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Database; Functional genomics; Jatropha curcas; Woody energy plant.
Affiliations: CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, The Innovative Academy of Seed Design, Chinese Academy of Sciences, Menglun, Mengla, Yunnan, 666303, China., College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China., Center of Economic Botany, Core Botanical Gardens, Chinese Academy of Sciences, Menglun, Mengla, Yunnan, 666303, China., CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, The Innovative Academy of Seed Design, Chinese Academy of Sciences, Menglun, Mengla, Yunnan, 666303, China. ., Center of Economic Botany, Core Botanical Gardens, Chinese Academy of Sciences, Menglun, Mengla, Yunnan, 666303, China. .

Abstract:  Background: Jatropha curcas is an oil-bearing plant, and has seeds with high oil content (~ 40%). Several advantages, such as easy genetic transformation and short generation duration, have led to the emergence of J. curcas as a model for woody energy plants. With the development of high-throughput sequencing, the genome of Jatropha curcas has been sequenced by different groups and a mass of transcriptome data was released. How to integrate and analyze these omics data is crucial for functional genomics research on J. curcas. Results: By establishing pipelines for processing novel gene identification, gene function annotation, and gene network construction, we systematically integrated and analyzed a series of J. curcas transcriptome data. Based on these data, we constructed a J. curcas database (JCDB), which not only includes general gene information, gene functional annotation, gene interaction networks, and gene expression matrices but also provides tools for browsing, searching, and downloading data, as well as online BLAST, the JBrowse genome browser, ID conversion, heatmaps, and gene network analysis tools. Conclusions: JCDB is the most comprehensive and well annotated knowledge base for J. curcas. We believe it will make a valuable contribution to the functional genomics study of J. curcas. The database is accessible at http://jcdb.xtbg.ac.cn. 

Retracted: No

PubPeer comments:
 This database is currently inaccessible. I find it odd that it has already been cited twice in Web of Science . Could the authors come forward for an explanation, please. , 
 I appreciate your interest in our work and apologize for the trouble you had caused. JCBD has migrated to http: jcdb.liu-lab.com . Wen Chen (chenwen@biochen.org) , 
 The URL in our [article] has been updated , 
 What the Editor-in-Chief of BMC Genomics has to say about this absurd fact? , 
 #4 New JCDB website: http: jcdb.liu-lab.com ,
CircPSMC3 suppresses the proliferation and metastasis of gastric cancer by acting as a competitive endogenous RNA through sponging miR-296-5p
Authors: Dawei Rong
Shuli Zhao
Betty Zhang
Hongyong Cao
Kai Fu
Weiwei Tang
Chen Lu
Journal: Molecular Cancer (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Gastric cancer; PTEN; Therapy; circPSMC3; miR-296-5p.
Affiliations: Department of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China., Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada., Department of General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. ., Department of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. .

Abstract:  Background: Circular RNAs (circRNAs) are a class of non-coding RNAs with a loop structure, but its functions remain largely unknown. Growing evidence has revealed that circRNAs play a striking role as functional RNAs in the progression of malignant disease. However, the precise role of circRNAs in gastric cancer (GC) remains unclear. Methods: CircRNAs were determined by human circRNA array analysis and quantitative reverse transcription polymerase reaction. Luciferase reporter, RNA pull down, and fluorescence in situ hybridization assays were employed to test the interaction between circPSMC3 and miR-296-5p. Ectopic over-expression and siRNA-mediated knockdown of circPSMC3, proliferation, migration and invasion in vitro, and in vivo experiment of metastasis were used to evaluate the function of circPSMC3. Results: CircPSMC3 rather than liner PSMC3 mRNA was down-regulated in GC tissues, corresponding plasmas from GC patients as well as GC cell lines compared to normal controls. Lower circPSMC3 expression in GC patients was correlated with higher TNM stage and shorter overall survival. Over-expression of circPSMC3 and miR-296-5p inhibitor could inhibit the tumorigenesis of gastric cancer cells in vivo and vitro whereas co-transfection of circPSMC3 and miRNA-296-5p could counteract this effect. Importantly, we demonstrated that circPSMC3 could act as a sponge of miR-296-5p to regulate the expression of Phosphatase and Tensin Homolog (PTEN), and further suppress the tumorigenesis of gastric cancer cells. Conclusion: Our study reveals that circPSMC3 can serve as a novel potential circulating biomarker for detection of GC. CircPSMC3 participates in progression of gastric cancer by sponging miRNA-296-5p with PTEN, providing a new insight into the treatment of gastric cancer. 

Retracted: No

PubPeer comments:
 Figure 3: More similar than expected. Could authors check please?  ,
Moracin M inhibits lipopolysaccharide-induced inflammatory responses in nucleus pulposus cells via regulating PI3K/Akt/mTOR phosphorylation
Authors: Yongjiang Zheng
Fang Guo
Yong Zou
Journal: International Immunopharmacology (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Intervertebral disc degeneration; LPS; Moracin M; PI3K/Akt/mTOR phosphorylation.
Affiliations: Department of Obstetrics & Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China., Department of Blood Transfusion, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China., Department of Hematology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, China. Electronic address: .

Abstract:  Moracin M, a phenolic component obtained from Mori Cortex, has been reported to have anti-inflammatory activities. The present study was designed to investigate the effects and mechanisms of Moracin M on lipopolysaccharide (LPS)-treated nucleus pulposus cells (NPCs) in intervertebral disc. NPCs were treated with moracin M at different concentrations for 1 h and then stimulated with LPS (0.5 Œºg/mL) for 24 h. The result demonstrated that moracin M could significantly inhibit LPS-induced inflammation. The elevated levels of IL-1Œ≤, TNF-Œ± and IL-6 induced by LPS could be reversed by moracin M in NPCs. Moreover, moracin M increased the expressions of autophagy-related proteins and up-regulated the phosphorylation of PI3K/Akt/mTOR in LPS-treated NPCs. In conclusion, our data demonstrated that moracin M might inhibit LPS-induced PI3K and Akt phosphorylation, which leading to promote the autophagy and inhibit the inflammatory mediator production in NPCs. 

Retracted: No

PubPeer comments:
 The results of Western blot in Figure 6 seem to have been mishandled. The membranes were seemed to be overexposured and the background is disappeared. Furthermore, the membrane of p-mTOR was seemed to splice and wipe.  , 
 Dear Cyrestis thyodamas , Your comment is highly appreciated. We are taking it seriously and are currently looking into the data associated with the question raised. Yongjiang zheng ,
Low-pass sequencing increases the power of GWAS and decreases measurement error of polygenic risk scores compared to genotyping arrays
Authors: Chase A Mazur
Tomaz Berisa
Joseph K Pickrell
Jeremiah H Li
Journal: Genome Research (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Low-pass sequencing; genotype imputation; genotyping arrays; trait mapping; polygenic scores
Affiliations: Gencove, Incorporated, New York, New York 10016, USA.

Abstract:  Low-pass sequencing (sequencing a genome to an average depth less than 1√ó coverage) combined with genotype imputation has been proposed as an alternative to genotyping arrays for trait mapping and calculation of polygenic scores. To empirically assess the relative performance of these technologies for different applications, we performed low-pass sequencing (targeting coverage levels of 0.5√ó and 1√ó) and array genotyping (using the Illumina Global Screening Array [GSA]) on 120 DNA samples derived from African- and European-ancestry individuals that are part of the 1000 Genomes Project. We then imputed both the sequencing data and the genotyping array data to the 1000 Genomes Phase 3 haplotype reference panel using a leave-one-out design. We evaluated overall imputation accuracy from these different assays as well as overall power for GWAS from imputed data and computed polygenic risk scores for coronary artery disease and breast cancer using previously derived weights. We conclude that low-pass sequencing plus imputation, in addition to providing a substantial increase in statistical power for genome-wide association studies, provides increased accuracy for polygenic risk prediction at effective coverages of ‚à?.5√ó and higher compared to the Illumina GSA. 

Retracted: No

PubPeer comments:
 Two panels from different papers appear to be the same.  Left-hand panel is from Figs 2C, 5b, 6c. Right-hand panel is from Fig 4B of [Dai et al (2020)] . Here in context:   There may be matches with other panels, or with panels of other papers within this oeuvre. ,
Mitomycin C induces fibroblast apoptosis and reduces intra-articular scar adhesion by regulating miR-21 and its target Programmed cell death 4
Authors: Jingcheng Wang
Hui Chen
Yu Sun
Shuguang Wang
Journal: Fitoterapia (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Fibroblast apoptosis; Intra-articular scar adhesion; Mitomycin C (MMC); Programmed cell death 4 (PDCD4); miR-21.
Affiliations: Dalian Medical University, Dalian, Liaoning, PR China., Department of Orthopedic Trauma, East Hospital, Tongji University School of Medicine, 150 Jimo Rd, 200120 Shanghai, PR China., Department of Orthopedics, Orthopedic Institute, Clinical Medical College of Yangzhou University, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, PR China. Electronic address: ., Dalian Medical University, Dalian, Liaoning, PR China; Department of Orthopedics, Orthopedic Institute, Clinical Medical College of Yangzhou University, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, PR China. Electronic address: .

Abstract:  Previous studies have shown that mitomycin C (MMC) can prevent scar adhesion after joint surgery, but the specific mechanism underlying this effect remains unclear. The purpose of this study was to explore the specific mechanism by which MMC promotes fibroblast apoptosis and prevents joint adhesion. The effect of MMC on fibroblasts was assessed using cell counting kit-8 (CCK-8) assays, western blotting, and TUNEL staining. We used qRT-PCR to measure the expression of miR-21 in fibroblasts treated with MMC. Luciferase activity assays were used to determine the relationships between miR-21 and Programmed cell death 4 (PDCD4). The effects of miR-21 and PDCD4 on fibroblast apoptosis were assessed using flow cytometry and western blotting. HE staining was used to determine the role of miR-21 in scar tissue formation in a model of joint adhesion. The results showed that MMC induced apoptosis of fibroblasts and decreased the expression of miR-21. Moreover, miR-21 down-regulation also induced apoptosis of fibroblasts. PDCD4 was confirmed to be a direct target of miR-21 by luciferase activity assay. The results from the animal model indicated that miR-21 attenuated the effect of MMC on reducing the number of fibroblasts. Our study shows that MMC can induce fibroblast apoptosis and prevent joint adhesion by regulating the expression of miR-21 and its target PDCD4. 

Retracted: No

PubPeer comments:
 Fig 3G.  The apoptotic rate of fibroblasts after different treatments was determined by flow cytometry .  There may be contamination between two panels, leading to identically-located points, which cancel out when one panel is black white-reversed and superimposed on the other.  ,
<p>Antitumor effects of Endostar(rh-endostatin) combined with gemcitabine in different administration sequences to treat Lewis lung carcinoma</p>
Authors: Shanshan Liu
Hongcheng Yue
Hongju Peng
Rongsheng Qin
Min Wu
Yunwei Han
Pan Huang
Yuan Li
Juan Fan
Journal: Cancer Management and Research (2019)
Discipline: CLINICAL MEDICINE
Keywords: antiangiogenic; combination therapy; gemcitabine; recombinant human endostatin.
Affiliations: The Oncology Department, Affiliated Hospital of Southwest Medical University, Lu Zhou, Si Chuan 646000, People's Republic of China., Neurology Department, Deyang People's Hospital, Deyang, Sichuan 618000, People's Republic of China.

Abstract:  Background: Endostatin therapy is known to efficiently inhibit angiogenesis and growth of endothelial cells. Nonetheless, the antitumor mechanisms of endostatin combined with chemotherapy remain to be elucidated. Methods: In our study, a Lewis lung carcinoma transplant mouse model was established and treated with the recombinant human [rh]-endostatin, Endostar, combined with gemcitabine at different sequences. 18F-FDG PET/CT imaging was performed to monitor tumor growth, and hypoxia was examined using an oxygen microelectrode. Vascular endothelial growth factor (VEGF) and alpha smooth muscle actin (Œ±-SMA) levels were detected via immunohistochemistry analysis and cell cycle distributions were analyzed by flow cytometry. Results: Endostar decreased VEGF expression, improved hypoxia, and influenced cell cycle distributions. Simultaneous treatment of Endostar and gemcitabine displayed significantly tumor inhibition, possessed the lowest uptake of FDG, improved oxygen partial pressure, decreased expression of VEGF, and increased pericyte coverage. Cell cycle analysis demonstrated that cells accumulated in the S phase following gemcitabine treatment and G0/G1 arrest occurred following Endostar treatment. An increase of cells in G0/G1 phase was observed following treatment with Endostar and gemcitabine. Conclusions: Our study suggests that the combination therapy of Endostar with gemcitabine simutaneously may optimally enhance their individual antitumor effects. 

Retracted: No

PubPeer comments:
 Figure 8 appears to have a repeated image. ***  ,
Role of the serine-threonine kinase PAK-1 in myxoma virus replication
Authors: Jennefer Masters
Grant McFadden
John W Barrett
Wei Zeng
Wen Chang
Fuan Wang
J B Johnston
Jingxin Cao
Melissa Mann
Che-Sheng Chung
Journal: Journal of Virology (2003)
Discipline: MICROBIOLOGY
Keywords: virus; signal transduction pathways; myxoma virus; 3T3 cells; serine-threonine kinases
Affiliations: Robarts Research Institute and Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, Canada N6G 2V4., Robarts Research Institute and Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, Canada N6G 2V4, Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan 115

Abstract:  Subversion or appropriation of cellular signal transduction pathways is a common strategy employed by viruses to promote an environment within infected cells that supports the viral replicative cycle. Using subsets of 3T3 murine fibroblasts previously shown to differ in their ability to support myxoma virus (MV) replication, we investigated the role of host serine-threonine kinases (STKs) as potential mediators of the permissive phenotype. Both permissive and nonpermissive 3T3 cells supported equivalent levels of virion binding, entry, and early virus gene expression, indicating that MV tropism in 3T3 cells was not determined by receptor-mediated entry. In contrast, late virus gene expression and viral DNA replication were selectively compromised in restrictive 3T3 cells. Addition of specific protein kinase inhibitors, many of which shared the ability to influence the activity of the STKs p21-activated kinase 1 (PAK-1) and Raf-1 attenuated MV replication in permissive 3T3 cells. Western blot detection of the phosphorylated forms of PAK-1 (Thr423) and Raf-1 (Ser338) confirmed activation of these kinases in permissive cells after MV infection or gamma interferon treatment, but the activated forms of both kinases were greatly reduced or absent in restrictive 3T3 cells. The biological significance of these activations was demonstrated by using the autoinhibitory domain of PAK-1 (amino acids 83 to 149), expression of which reduced the efficiency of MV infection in permissive 3T3 cells concurrent with a decrease in PAK-1 activation. In comparison, overexpression of a constitutively active PAK-1 (T423E) mutant increased MV replication in restrictive 3T3 cells. These observations suggest that induced signaling via cellular STKs may play important roles in determining the permissiveness of host cells to poxvirus infection. 

Retracted: No

PubPeer comments:
 Figure 4. Much more similar than expected.  ,
Notice of Violation of IEEE Publication Principles Nuclear Localization of HIV-1 Tat Functionalized Gold Nanoparticles
Authors: S Wai Ling Chu
J M de la Fuente
A S G Curtis
M Mullin
C C Berry
Journal: IEEE Transactions on NanoBioscience (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: cell plasma membrane; macromolecules; cell penetrating peptides; protein transduction domains; intracellular delivery
Affiliations: Centre for Cell Engineering, Institute of Biomedical and Life Sciences, University of Glasgow, UK. 

Abstract:  The impermeable nature of the cell plasma membrane limits the therapeutic uses of many macromolecules and there is therefore a growing effort to circumvent this problem by designing strategies for targeted intracellular delivery. During the last decade several cell penetrating peptides, such as the HIV-1 tat peptide, have been shown to traverse the cell membrane, where integral protein transduction domains (PTDs) are responsible for their cellular uptake, and to reach the nucleus while retaining biological activity. It has since been discovered that PTDs can enable the cellular delivery of conjugated biomolecules and even nanoparticles, but nuclear delivery has remained problematic. This present study focuses on the development of water soluble, biocompatible gold nanoparticles of differing size functionalized with the HIV-1 tat PTD with the aim of producing nuclear targeting agents. The particles were subsequently tested in vitro with a human fibroblast cell line, with results demonstrating successful nanoparticle transfer across the plasma membrane, with 5 nm particles achieving nuclear entry while larger 30 nm particles are retained in the cytoplasm, suggesting entry is blocked via nuclear pores dimensions. 

Retracted: No

PubPeer comments:
 Identified by another reader. Both papers: https: pubpeer.com publications BB625E026960B628B341FBB9ACE318 https: pubpeer.com publications 7F0C9D7095FB709B597250DAF82108 ***  ,
KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling
Authors: Stephen P Jackson
Abderrahmane Kaidi
Journal: Nature (2013)
Discipline: Multidisciplinary
Keywords: DNA lesions; chromatin sensing; DNA-damage signalling; tyrosine phosphorylation; KAT5
Affiliations: The Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.

Abstract:  The detection of DNA lesions within chromatin represents a critical step in cellular responses to DNA damage. However, the regulatory mechanisms that couple chromatin sensing to DNA-damage signalling in mammalian cells are not well understood. Here we show that tyrosine phosphorylation of the protein acetyltransferase KAT5 (also known as TIP60) increases after DNA damage in a manner that promotes KAT5 binding to the histone mark H3K9me3. This triggers KAT5-mediated acetylation of the ATM kinase, promoting DNA-damage-checkpoint activation and cell survival. We also establish that chromatin alterations can themselves enhance KAT5 tyrosine phosphorylation and ATM-dependent signalling, and identify the proto-oncogene c-Abl as a mediator of this modification. These findings define KAT5 tyrosine phosphorylation as a key event in the sensing of genomic and chromatin perturbations, and highlight a key role for c-Abl in such processes. 

Retracted: Yes

PubPeer comments:
 Retracted https: retractionwatch.com 2019 04 11 authors-have-papers-in-nature-and-science-retracted-on-the-same-day , 
 2019 retraction note. https: www.nature.com articles s41586-019-1142-2 The authors are retracting this Article to correct the scientific literature, owing to issues with figure presentation and underlying data. The authors cannot confirm the results in the affected figures and thus wish to retract the Article in its entirety. Both authors, Abderrahmane Kaidi and Stephen P. Jackson, agree with the Retraction. ,
Selective depletion of inducible HSP70 enhances immunogenicity of rat colon cancer cells
Authors: C Garrido
M J√§√§ttel√§
A Parcellier
A Fromentin
F Martin
E Solary
J M Bruey
N Larmonier
S Gurbuxani
Journal: Oncogene (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HSP70; tumor cells; immunogenicity; PRO colon cancer cell; immune response
Affiliations: INSERM 517, IFR 100, Faculty of Medicine, 7 Boulevard Jeanne d'Arc, 21033 Dijon, France.

Abstract:  Expression of inducible heat shock protein 70 (HSP70) in tumor cells has been proposed to enhance their immunogenicity. However, HSP70 has also been demonstrated to prevent tumor cell death, a key process for the development of tumor cell immunogenicity. In the present study, we investigated the influence of the HSP70 protein level on PRO colon cancer cell growth and immunogenicity in syngeneic BDIX rats and nude mice. These cells have a basal expression of HSP70 which can be substantially increased by heat shock. When injected subcutaneously in syngeneic animals, PRO cells do not induce any detectable immune response and give rise to progressive, metastatic and lethal tumors. Stable transfection of an anti-sense hsp70 cDNA in PRO cells (PRO-70AS cells) strongly decreased HSP70 expression and sensitized cell-free extracts to cytochrome c/dATP-mediated activation of caspases. Subcutaneous injection of PRO-70AS cells induced tumors that rapidly regressed in syngeneic rats while they grew normally in nude mice. Syngeneic rats injected with PRO-70AS cells became protected against a further challenge with PRO cells. The tumor-specific immune response induced by HSP70-depleted PRO-70AS cells was associated with an increased rate of cell death in vivo. These PRO-70AS cells were also more sensitive to NO-mediated, caspase-dependent, macrophage cytotoxicity in vivo. Altogether, these results indicate that reduced level of HSP70 expression in PRO- colon cancer cells results in the generation of a specific immune response by promoting cell death in vivo. 

Retracted: No

PubPeer comments:
 Figure 1. Splices HSP70 panel, no splices HSC70 panel.  ,
Glutathione-s-transferase A 4 (GSTA4) suppresses tumor growth and metastasis of human hepatocellular carcinoma by targeting AKT pathway
Authors: Xun Yang Liu
Jin Hui Yang
Wan Pin Nie
Chuang Peng
Bo Jiang
Chu Ping Liu
Chang Jun Liu
Mei Fu Chen
Jin Shu Wu
Fei Zhou Huang
Xin Min Yin
Xian Hai Mao
Xian Bo Shen
Journal: American journal of translational research (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: AKT; GSTA4; hepatocellular carcinoma; metastasis.
Affiliations: Department of General Surgery, The Third Xiangya Hospital of Central South University410013, Changsha, Hunan, China; Department of Hepatobiliary Surgery Hunan People's Hospital410005, Changsha, Hunan, China., Department of Hepatobiliary Surgery Hunan People's Hospital 410005, Changsha, Hunan, China., Department of General Surgery, The Third Xiangya Hospital of Central South University 410013, Changsha, Hunan, China.

Abstract:  Hepatocellular carcinoma (HCC) is one of the most lethal malignancies of cancers and its prognosis remains dismal due to the paucity of effective therapeutic targets. Up-regulation of glutathione-s-transferase A 4 (GSTA4) is associated with poor prognosis of HCC, but its functional mechanism in HCC remains unclear. In this study, we investigated the roles of GSTA4 in tumor growth and metastasis of HCC and found that GSTA4 was frequently up-regulated in HCC tissues. Through gain- and loss-of-function studies, GSTA4 was demonstrated to significantly regulate cell proliferation, migration, and invasion in vitro. Furthermore, GSTA4 overexpressing significantly promoted the tumorigenicity and metastasis of HCC cells in nude mice models bearing human HCC, whereas silencing endogenous GSTA4 caused an opposite outcome. Moreover, we demonstrated that GSTA4 enhanced HCC aggressiveness by activating protein kinase B (AKT) signaling. In multivariate analysis, our results GSTA4 overexpression promotes the progression of hepatocellular carcinoma and might represent a novel therapeutic target for its treatment. 

Retracted: No

PubPeer comments:
 Liu CJ, Yang JH, Huang FZ, et al. Glutathione-s-transferase A 4 (GSTA4) suppresses tumor growth and metastasis of human hepatocellular carcinoma by targeting AKT pathway. Am J Transl Res. 2017;9(2):301-315. Published 2017 Feb 15.  **The title of contrary to the abstract and experimental results**.The title of the article is GSTA4 suppresses tumor growth and metastasis of human hepatocellular carcinoma,but the result of article is  GSTA4 overexpressing significantly promoted the tumorigenicity and metastasis of HCC cells . **In addition, the article repeatedly appeared results completely unrelated to the study disease description**uff0cexample in supplementary figure 1A authors find that  Oncomine analysis of neoplastic vs. normal tissue showed that GSTA4 were significantly overexpressed in different types of **lung cancer** in different datasets . ,
Nobiletin, a citrus polymethoxy flavonoid, suppresses gene expression and production of aggrecanases-1 and -2 in collagen-induced arthritic mice
Authors: Takashi Sato
Aiping Lu
Weiheng Chen
Chunfang Liu
Na Lin
Masamichi Yano
Akira Ito
Keisuke Imada
Journal: Biochemical and biophysical research communications (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Aggrecanase-1; ADAMTS-4; ADAMTS-5; cartilage destruction; rheumatoid arthritis
Affiliations: Department of Biochemistry and Molecular Biology, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji-shi, Tokyo 192-0392, Japan.  <>

Abstract:  Aggrecanase-1/a disintegrin and metalloproteinase with thrombospondin-like motifs (ADAMTS)-4 and aggrecanase-2/ADAMTS-5 have been shown to play crucial roles in cartilage destruction in arthritic diseases, including rheumatoid arthritis and osteoarthritis. In this study, we examined the effects of nobiletin, a citrus polymethoxy flavone, on the expression and production of ADAMTS-4 and -5 in vitro and in vivo. Nobiletin (16-64muM) interfered with the interleukin (IL)-1beta-mediated ADAMTS-4 and -5 mRNA expression in cultured human synovial fibroblasts. Furthermore, intraperitoneal administration of nobiletin (15, 30, and 60mg/kg) also suppressed ADAMTS-4 and -5 mRNA expression in the joint tissues of collagen-induced arthritic (CIA) mice. Immunohistochemical analysis using an antibody against aggrecan neoepitope (NVTEGE(373)) revealed that aggrecanase-mediated degradation of aggrecan in cartilage was effectively inhibited by nobiletin. These results provide novel evidence that nobiletin effectively interferes with gene expression of ADAMTS-4 and -5, and thereby prevents cartilage destruction in CIA mice. 

Retracted: No

PubPeer comments:
 Fig. 3 D.  Histological evaluation of the joint tissues of CIA mice treated with nobiletin. Paraffin sections of ankle (A,C) and **knee (B,D**) joints were stained with hematoxylin and eosin, and joint histology was evaluated. (A,B) Sections from vehicle-treated mice. (C,**D) Sections from nobiletin** (60 mg kg)-treated mice. Here rotated through 90 deg:  The image previously appeared as a Control in Fig 1C of [Lin et al (2007)] .  Fig. 1 u2013 Effects of triptolide on arthritis progression and joint histology of CIA mice. Mice were orally administered triptolide (Trip) or vehicle for 21 days from the first day of the onset of the clinical symptoms of arthritis. At the end of the experiment, the clinical onset and histology of the joints were evaluated. ... (C) displays histological observation of the joints in mice. In **normal mice**, there is normal knee joint architecture...  ,
Retracted : Suppression of long non‚Äêcoding RNA LET potentiates bone marrow‚Äêderived mesenchymal stem cells (BMSCs) proliferation by up‚Äêregulating TGF‚ÄêŒ?
Authors: Zhiliang Zhang
Yi Lu
Zhihong Fan
Xin Jin
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cell proliferation; LncRNA low expression in tumor; Wnt/Œ≤-catenin pathway; bone marrow stem cells; transforming growth factor Œ≤1.
Affiliations: Department of Plastic Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Abstract:  Long non coding RNAs (lncRNAs) show an encouraging trend in regulating the proliferation of bone marrow-derived mesenchymal stromal cells (BMSCs). The present study investigated the role of lncRNA low expression in tumor (LET) in BMSCs proliferation. Our result showed that LET was down-regulated in rapidly proliferated BMSCs (P &lt; 0.05). Suppression of LET promoted BMSCs proliferation and over-expression of LET inhibited BMSCs proliferation (P &lt; 0.05). LET negatively regulated the expression of transforming growth factor Œ≤1 (TGF-Œ≤1) in BMSCs (P &lt; 0.05). Knockdown of TGF-Œ≤1 reversed the LET suppression-induced BMSCs proliferation (P &lt; 0.05). Moreover, knockdown of TGF-Œ≤1 alleviated the LET suppression-induced activation of Wnt/Œ≤-catenin pathway in BMSCs. Therefore, we drew the conclusion that LET suppression promoted BMSCs proliferation by up-regulating the expression of TGF-Œ≤1 and activating Wnt/Œ≤-catenin pathway. 

Retracted: Yes

PubPeer comments:
 Figure 6, SEM micrograph of ***Phyllanthus emblica*** embedded silver nanoparticles has been published two [years later](http: pubpeer.com publications 207C74F821B86AE5FEE54CCD9EA293) by the same group for ***Carissa carandas*** (another plant) embedded silver nanoparticles (red boxes). Could the authors please comment? Of note, this group has many articles with similar issues: https: pubpeer.com search?q=Vikas+Kumar https: pubpeer.com search?q=amita+verma  , 
 Figure 15f (DEN-induced + Silymarin treatment) overlaps with Figure 9a (normal control) of another paper by the same group published a year before (blue boxes). Images have different vertical sizes. Could the authors please comment?  , 
 Another lovely sighting: Figure 7b describes TEM images of synthesized ***Phyllanthus emblica*** silver nanoparticles (PEAgNPs), while same image (red boxes, resized) was described a year before in [Singh et al. 2018 IET Nanobiotechnol](http: pubpeer.com publications D36220A66B2748514D09FB87FDE206#1) as biofabricated silver nanoparticles AgNPs by using ***Carissa carandas*** leaves.  ,
Normal host prion protein (PrPC) is required for scrapie spread within the central nervous system
Authors: M Fischer
T Bl√§ttler
A Raeber
S Brandner
A Sailer
A Aguzzi
C Weissmann
Journal: Proceedings of the National Academy of Sciences of the United States of America (1996)
Discipline: Multidisciplinary
Keywords: PrPC; scrapie; prion; neurograft; intraocular
Affiliations: Institute of Neuropathology, University Hospital, Z√ºrich, Switzerland.

Abstract:  Mice devoid of PrPC (Prnp%) are resistant to scrapie and do not allow propagation of the infectious agent (prion). PrPC-expressing neuroectodermal tissue grafted into Prnp% brains but not the surrounding tissue consistently exhibits scrapie-specific pathology and allows prion replication after inoculation. Scrapie prions administered intraocularly into wild-type mice spread efficiently to the central nervous system within 16 weeks. To determine whether PrPC is required for scrapie spread, we inoculated prions intraocularly into Prnp% mice containing a PrP-overexpressing neurograft. Neither encephalopathy nor protease-resistant PrP (PrPSc) were detected in the grafts for up to 66 weeks. Because grafted PrP-expressing cells elicited an immune response that might have interfered with prion spread, we generated Prnp% mice immunotolerant to PrP and engrafted them with PrP-producing neuroectodermal tissue. Again, intraocular inoculation did not lead to disease in the PrP-producing graft. These results demonstrate that PrP is necessary for prion spread along neural pathways. 

Retracted: No

PubPeer comments:
 Figure 1e and 1f is very similar to a Figure published previously by the same group.  ,
The early-immediate gene EGR-1 is induced by transforming growth factor-beta and mediates stimulation of collagen gene expression
Authors: Shu-Jen Chen
John Varga
Yasuji Mori
Hongyan Ning
Snezna Sodin-Semrl
Shinsuke Takagawa
Wataru Ishida
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Transforming growth factor-beta; TGF-beta; collagen synthesis; Smad signaling pathway; type I procollagen gene
Affiliations: Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.

Abstract:  Transforming growth factor-beta (TGF-beta) stimulates collagen synthesis and accumulation, and aberrant TGF-beta signaling is implicated in pathological organ fibrosis. Regulation of type I procollagen gene (COL1A2) transcription by TGF-beta involves the canonical Smad signaling pathway as well as additional protein and lipid kinases, coactivators, and DNA-binding transcription factors that constitute alternate non-Smad pathways. By using Affymetrix microarrays to detect cellular genes whose expression is regulated by Smad3, we identified early growth response factor-1 (EGR-1) as a novel Smad3-inducible gene. Previous studies implicated Egr-1 in cell growth, differentiation, and survival. We found that TGF-beta induced rapid and transient accumulation of Egr-1 protein and mRNA in human skin fibroblasts. In transient transfection assays, TGF-beta stimulated the activity of the Egr-1 gene promoter, as well as that of a minimal Egr-1-responsive reporter construct. Furthermore, TGF-beta enhanced endogenous Egr-1 interaction with a consensus Egr-1-binding site element and with GC-rich DNA sequences of the human COL1A2 promoter in vitro and in vivo. Forced expression of Egr-1 by itself caused dose-dependent up-regulation of COL1A2 promoter activity and further enhanced the stimulation induced by TGF-beta. In contrast, the TGF-beta response was abrogated when the Egr-1-binding sites of the COL1A2 promoter were mutated or deleted. Furthermore, Egr-1-deficient embryonic mouse fibroblasts showed attenuated TGF-beta responses despite intact Smad activation, and forced expression of ectopic EGR-1 in these cells could restore COL1A2 stimulation in a dose-dependent manner. Taken together, these findings identify Egr-1 as a novel intracellular TGF-beta target that is necessary for maximal stimulation of collagen gene expression in fibroblasts. The results therefore implicate Egr-1 in the profibrotic responses elicited by TGF-beta and suggest that Egr-1 may play a new and important role in the pathogenesis of fibrosis. 

Retracted: No

PubPeer comments:
  Multiple undeclared splicing sites in the immunoblots in Figure 2A. ,
Highly monodisperse Pt(0)@AC NPs as highly efficient and reusable catalysts: the effect of the surfactant on their catalytic activities in room temperature dehydrocoupling of DMAB
Authors: Bet√ºl √áelik
Esma Erken
Sinan Eri≈ü
Yunus Yƒ±ldƒ±z
Birg√ºtay ≈ûahin
Handan Pamuk
Fatih Sen
Journal: Catalysis Science & Technology (2016)
Discipline: CHEMISTRY
Keywords: Pt(0) nanoclusters; dehydrocoupling; dimethylamine‚Äìborane; hydrogen storage materials; reduction
Affiliations: Sen Research Group, Biochemistry Department, Faculty of Arts and Sciences, Dumlupƒ±nar University, Evliya √áelebi Campus

Abstract: Addressed herein, we report the development of highly efficient and monodisperse Pt(0) nanoclusters for the dehydrocoupling of dimethylamine‚Äìborane (DMAB) which is considered to be one of the new hydrogen storage materials. The prepared Pt(0) nanoclusters were in situ generated for the first time from the reduction of PtCl4 and use of dipentylamine (DPA) and tripentylamine (TPA) ligands on activated carbon for the dehydrocoupling of dimethylamine‚Äìborane at room temperature and characterized by ICP-OES, XRD, TEM, HR-TEM, AFM, EDX, and XPS techniques. All the results show that highly crystalline and stable colloidal Pt(0)/DPA@AC and Pt(0)/TPA@AC nanoparticles have been formed and Pt(0)/DPA@AC and Pt(0)/TPA@AC were found to be two of the most active and long-lived catalysts with superior reusability performance in the dehydrocoupling of DMAB at room temperature.

Retracted: Yes

PubPeer comments:
 Image concerns in this paper were found during a systematic search of papers in Spandidos journals for possible duplicated images. Figure 1D. * Red boxes: In the 0h row, the  Scramble and  mimic panels appear to shown an overlap.  ,
Corrigendum: Akt2 Regulates the Differentiation and Function of NKT17 Cells via FoxO-1-ICOS Axis
Authors: Lisa S Westerberg
Yukai Jing
Xingtian Xuan
Chaohong Liu
Jinzhi Wang
LinLin Niu
Liling Li
Di Yang
Journal: Frontiers in Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: Akt2; FoxO-1; ICOS; NKT17; iNKT.
Affiliations: Chongqing Key Laboratory of Child Infection and Immunity, Chongqing, China., Department of Pediatric Research Institute, Children's Hospital of Chongqing Medical University, Chongqing, China., Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China., Department of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China., Department of Microbiology Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.

Abstract:  [This corrects the article DOI: 10.3389/fimmu.2018.01940.]. 

Retracted: Yes

PubPeer comments:
 2020 Expression of Concern. https: www.tandfonline.com doi full 10.1080 0886022X.2020.1752428 The Editors and Publisher of Renal Failure wish to issue an expression of concern for the published article. Jing Xue, Liang Wang, Cai-Mei Chen, Jing-Yu Chen Zhu-Xing Sun. Acute kidney injury influences mortality in lung transplantation. Renal Failure. 2014;36(4):541u2013545. https: doi.org 10.3109 0886022X.2013.876350. Concerns have been raised that the study described in the article did not adhere to ethical guidelines as outlined in the Declaration of Helsinki and the Declaration of Istanbul and guidance from the World Health Organization and the World Medical Association regarding the source of transplanted human organs. Specifically, the British Medical Journal Open (BMJ Open) published an article highlighting many papers in which there is concern that transplanted organs were harvested from executed prisoners in China. In response to these concerns, we contacted the authors to clarify the source of the transplanted organs received by the patients described in their study. However, despite multiple attempts to contact the authors and their institutions, no response was received. The Editors of Renal Failure would like to alert readers of this. We will provide an update if we receive any further information. Renal Failure publishes research adhering to internationally accepted ethical standards and is committed to upholding the Declaration of Helsinki and Declaration of Istanbul. Taylor Francis endorses the ethics guidelines described by the World Health Organization (WHO) and the World Medical Association (WMA). ,