PReD-Bench/PRed-Bench huggingface dataset:
Lipid signalling couples translational surveillance to systemic detoxification in Caenorhabditis elegans
Authors: Peter Breen
Eleftherios Mylonakis
J Amaranath Govindan
Xinrui Zhang
Jonah Larkins-Ford
Gary Ruvkun
Elamparithi Jayamani
Journal: Nature Cell Biology (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Translation; eukaryotes; toxins; virulence factors; defence pathways
Affiliations: Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA., Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA., Division of Infectious Diseases, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, Rhode Island 02903, USA.

Abstract:  Translation in eukaryotes is followed to detect toxins and virulence factors and coupled to the induction of defence pathways. Caenorhabditis elegans germline-specific mutations in translation components are detected by this system to induce detoxification and immune responses in distinct somatic cells. An RNA interference screen revealed gene inactivations that act at multiple steps in lipid biosynthetic and kinase pathways upstream of MAP kinase to mediate the systemic communication of translation defects to induce detoxification genes. Mammalian bile acids can rescue the defect in detoxification gene induction caused by C. elegans lipid biosynthetic gene inactivations. Extracts prepared from C. elegans with translation deficits but not from the wild type can also rescue detoxification gene induction in lipid-biosynthesis-defective strains. These eukaryotic antibacterial countermeasures are not ignored by bacteria: particular bacterial species suppress normal C. elegans detoxification responses to mutations in translation factors. 

Retracted: No

PubPeer comments:
 I enjoyed very much reading this article. However, I found some possible concerns with images that authors might want to comment about 1) It seems that the first panel of Figure 1a was reused at least three times in the article (Figure 1a twice and as control in Supplementary Fig. 1c, which does not mention the use of RNAi, so Iu2019m supposing it canu2019t be the same worms as Figure 1a). ![file] 2) In Supplementary Fig. 1i, almost all worms has the **same** pattern when you compare eft-4 RNAi on hypodermis-restricted strain (pgp-5::gfp) vs eft-4 RNAi on neuron-restricted strain (pgp-5::gfp). The authors might agree that this is a little unexpected, and maybe it might be worth it to check the original files. ![file] ,
Long non‐coding RNA highly up‐regulated in liver cancer promotes epithelial‐to‐mesenchymal transition process in oral squamous cell carcinoma
Authors: Shuai Sun
Jing Tang
Hongyu Yang
Wen Su
Yuehong Shen
Yufan Wang
Journal: Journal of Cellular and Molecular Medicine (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: epithelial-to-mesenchymal transition; highly up-regulated in liver cancer; long non-coding RNA; oral squamous cell carcinoma.
Affiliations: Department of Oral and Maxillofacial Surgery Peking University Shenzhen Hospital Shenzhen Guangdong China, Peking University Shenzhen Hospital Clinical College, Anhui Medical University Hefei Anhui China, Jingzhou Central Hospital Jingzhou Hubei

Abstract:  Oral squamous cell carcinoma (OSCC) is an oral and maxillofacial malignancy that exhibits high incidence worldwide. In diverse human cancers, the long non-coding RNA (lncRNA) highly up-regulated in liver cancer (HULC) is aberrantly expressed, but how HULC affects OSCC development and progression has remained mostly unknown. We report that HULC was abnormally up-regulated in oral cancer tissues and OSCC cell lines, and that suppression of HULC expression in OSCC cells not only inhibited the proliferation, drug tolerance, migration and invasion of the cancer cells, but also increased their apoptosis rate. Notably, in a mouse xenograft model, HULC depletion reduced tumorigenicity and inhibited the epithelial-to-mesenchymal transition process. Collectively, our findings reveal a crucial role of the lncRNA HULC in regulating oral cancer carcinogenesis and tumour progression, and thus suggest that HULC could serve as a novel therapeutic target for OSCC. 

Retracted: No

PubPeer comments:
 FIGURE4A AND FIGURE4B seem that the picture is duplicated![file] ,
MicroRNA‑876‑5p inhibits the progression of glioblastoma multiforme by directly targeting Forkhead box M1
Authors: Jia Lu
Hong Zhang
Zhigang Sun
Lina Wang
Xueman Lyu
Journal: Oncology Reports (2018)
Discipline: CLINICAL MEDICINE
Keywords: miRNA-876-5p; glioblastoma multiforme; FOXM1; dysregulation; therapeutic target
Affiliations: Department of Ophthalmology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China., Department of Neurosurgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.

Abstract:  Considerable evidence has suggested that microRNAs (miRNAs) are dysregulated in glioblastoma multiforme (GBM), and their dysregulation may modulate the aggressiveness of GBM. Therefore, miRNAs with dysregulated expression are potential therapeutic targets for the treatment of GBM. miRNA‑876‑5p (miR‑876‑5p) has recently been identified to be aberrantly expressed and serve an important role in hepatocellular carcinoma and lung cancer. However, its expression pattern and functional significance in GBM remains largely unknown. Therefore, the present study detected miR‑876‑5p expression in GBM, examined the biological roles of miR‑876‑5p in GBM progression and explored its underlying mechanism. The present study demonstrated that miR‑876‑5p expression was significantly downregulated in GBM tissues and cell lines. Overexpression of miR‑876‑5p restricted the proliferation, induced the apoptosis and reduced the migration and invasion capabilities of GBM cells. In GBM cells, Forkhead box M1 (FOXM1) was identified as a direct target of miR‑876‑5p. FOXM1 was overexpressed in clinical GBM tissues, and its overexpression was inversely correlated with miR‑876‑5p level. Small interfering RNA‑mediated knockdown of FOXM1 exhibited effects similar to those of miR‑876‑5p overexpression in GBM cells. The tumour suppressive roles of miR‑876‑5p overexpression in GBM cells were significantly reversed by FOXM1 reintroduction. Overall, the present results revealed that miR‑876‑5p may inhibit the development of GBM by directly targeting FOXM1, suggesting that this miRNA may be a potential therapeutic target in patients, for the management of GBM. 

Retracted: Yes

PubPeer comments:
 This paper was one of many listed as the work of a papermill, on account of its stylistic features. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit#gid=0 Some time in the last week or so, the journal wished it into the cornfield: https: www.europeanreview.org article 22236 Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, u201cMiR-100 up-regulation enhanced cell autophagy and apoptosis induced by cisplatin in osteosarcoma by targeting mTOR, by Z. Yu, N. Li, K. Jiang, N. Zhang, L.-L. Yao, published in Eur Rev Med Pharmacol Sci 2018; 22 (18): 5867-5873u2013DOI: 10.26355 eurrev_201809_15913 u2013PMID: 30280766u201d has been withdrawn. The Publisher apologizes for any inconvenience this may cause. ,
A new effector pathway links ATM kinase with the DNA damage response
Authors: Constantinos Demonacos
Linda Smith
Martin Jansson
Nicholas B La Thangue
Marija Krstic-Demonacos
Danmei Xu
Darran P O&#x27;Connor
Journal: Nature Cell Biology (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ATM kinase; ATR kinase; DNA damage response; Strap; phosphorylation
Affiliations: Division of Biochemistry and Molecular Biology, Davidson Building, University of Glasgow, Glasgow G12 8QQ, UK.

Abstract:  The related kinases ATM (ataxia-telangiectasia mutated) and ATR (ataxia-telangiectasia and Rad3-related) phosphorylate a limited number of downstream protein targets in response to DNA damage. Here we report a new pathway in which ATM kinase signals the DNA damage response by targeting the transcriptional cofactor Strap. ATM phosphorylates Strap at a serine residue, stabilizing nuclear Strap and facilitating formation of a stress-responsive co-activator complex. Strap activity enhances p53 acetylation, and augments the response to DNA damage. Strap remains localized in the cytoplasm in cells derived from ataxia telangiectasia individuals with defective ATM, as well as in cells expressing a Strap mutant that cannot be phosphorylated by ATM. Targeting Strap to the nucleus reinstates protein stabilization and activates the DNA damage response. These results indicate that the nuclear accumulation of Strap is a critical regulator in the damage response, and argue that this function can be assigned to ATM through the DNA damage-dependent phosphorylation of Strap. 

Retracted: No

PubPeer comments:
 Figure 1e. Vertical changes in signal in P-Ser 203 Strap and p53 panels, but not in PCNA panel. ![file] ,
Chlorogenic acid inhibits proliferation in human hepatoma cells by suppressing noncanonical NF-κB signaling pathway and triggering mitochondrial apoptosis
Authors: Yanfei Jiang
Juane Dong
Na Shi
Hao Nan
Hongying Chen
Wenfang Hao
Journal: Molecular Biology Reports (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Apoptosis; Chlorogenic acid; Hepatocellular carcinoma; Transcriptome; Viability.
Affiliations: College of Life Sciences, Northwest A & F University, Yangling, 712100, Shaanxi, China., College of Chemistry & Pharmacy, Northwest A & F University, Yangling, 712100, Shaanxi, China., College of Life Sciences, Northwest A & F University, Yangling, 712100, Shaanxi, China. .

Abstract:  Chlorogenic acid (CGA), a phenylpropanoid derived from Eucommia ulmoides Oliver, has been shown to exhibit potent cytotoxic and anti-proliferative activities against several human cancers. However, the effects of CGA on hepatocellular carcinoma (HCC) and the underlying mechanisms have not been intensively studied. In this study, the CGA treatment effects on the viability of human hepatoma cells were investigated by MTT assay. Our data showed that CGA could dose-dependently inhibit the activity of human hepatoma cells Hep-G2 and Huh-7, but did not affect the activity and growth of normal human hepatocyte QSG-7701. The genes and pathways influenced by CGA treatment were explored by RNA sequencing and bioinformatics analysis, which identified 323 differentially expressed genes (DEGs) involved in multiple pharmacological signaling pathways such as MAPK, NF-κB, apoptosis and TGF-β signaling pathways. Further analyses by real-time quantitative PCR, Western blot and flow cytometry revealed that CGA effectually suppressed the noncanonical NF-κB signaling pathway, meanwhile it activated the mitochondrial apoptosis of HCC by upregulation of the BH3-only protein Bcl-2 binding component 3 (BBC3). Our findings demonstrated the potential of CGA in suppressing human hepatoma cells and provided a new insight into the anti-cancer mechanism of CGA. 

Retracted: No

PubPeer comments:
 One of the cell lines used in this paper is QSG-7701. It is stated to be a  normal human hepatocyte . But unfortunatly it is a HeLa contaminated cell line. This means that some of the conclusions of this study such as  Taken together, we found in this study that chlorogenic acid exhibited selective inhibition activity in hepatoma cells compared with normal human hepatocytes are unfortunatly incorrect: the comparison was carried out between 2 hepatoma cell lines and an endocervical adenocarcinoma cell line. See: [The relevant Cellosaurus entry] ,
WITHDRAWN: Increase in phosphorylation of PDK1 and cell survival after acute spinal cord injury
Authors: Ye Huang
Jianhua Cao
Aiguo Shen
Gan Shen
Yi Zhong
Xiang Lu
Meijiang Feng
Xiaowei Yu
Journal: Journal of the neurological sciences (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: accidental duplication; published article; withdrawn
Affiliations: Department of Orthopaedics, The Second Affiliated Hospital, Nanjing Medical University, Nanjing 210011, China.

Abstract:  The Publisher regrets that this article is an accidental duplication of an article that has already been published, doi:10.1016/j.jns.2012.06.003. The duplicate article has therefore been withdrawn. 

Retracted: No

PubPeer comments:
  The Publisher regrets that this article is an accidental duplication of an article that has already been published, doi:https: doi.org 10.1016 j.jns.2012.06.003. The duplicate article has therefore been withdrawn. ,
Curcumin down regulates smokeless tobacco-induced NF-kappaB activation and COX-2 expression in human oral premalignant and cancer cells
Authors: Jatinder Kaur
Bharat B Aggarwal
Shishir Shishodia
Chhavi Sharma
Ranju Ralhan
Journal: Toxicology (2006)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Smokeless tobacco; oral cancer; South East Asia; India; nuclear factor-kappaB
Affiliations: Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.

Abstract:  Smokeless tobacco (ST) consumption is a major cause of oral cancer in South East Asia including India. Recently, we showed that exposure to smokeless tobacco extract (STE) (khaini) results in increased expression and activation of nuclear factor-kappaB (NF-kappaB) and its downstream target cyclooxygenase-2 (COX-2) in human oral cell systems in vitro. The present study was designed to test the hypothesis that curcumin may inhibit the activation of NF-kappaB in ST exposed oral premalignant and cancer cells. Exposure of oral premalignant and cancer cells to curcumin resulted in significant decrease in cell viability and induced apoptosis. STE-induced nuclear translocation and DNA-binding activity of NF-kappaB were inhibited in curcumin pretreated oral premalignant and cancer cells in vitro. Curcumin treatment led to decreased expression of NF-kappaB and COX-2. The tobacco specific nitrosamine, 4-(methylnitrosamino-)-1-(3-pyridyl)-1-butanone (NNK), is one of the carcinogenic components of STE (khaini). We demonstrate that curcumin pretreatment abrogated NNK-induced activation of NF-kappaB and COX-2 expression, suggesting that NNK is one of the factors in STE (khaini) modulated by curcumin. In conclusion, our findings demonstrate for the first time that curcumin downregulates STE (khaini) or NNK-induced NF-kappaB and COX-2 in oral premalignant and cancer cells in vitro. 

Retracted: No

PubPeer comments:
 The migration invasion assays of this paper have what appear to be numerous image duplications or partial image duplications. Some of these may have been treated the same (its a little unclear what the  NC miRNA used is), but some are definitely given different treatments. For example in figure 3E and 2C, in the invasion assay of the AGS cells, the same partial image is labeled as both NC and mir-188-5p mimic (light gray boxes). ![file] , 
 Dear PUBPEER administrator, Thank you very much for your email notice of July 23, 2020 regarding image duplication errors identified in our article published in BMC Cancer 19(1):505, 2019; DOI: https: doi.org 10.1186 s12885-019-5731-0. Upon receipt of your comment, we have responded immediately by sending an erratum where all the indicated errors were corrected to the journal waiting for the correction to be published. We have done a thorough investigation into the mistake and identified that there was an inadvertent mistake made in the process of transferring data pictures taken from the microscopy system. We are most grateful to PUBPEER for careful review of our paper and for noting these errors. Warmest regards, Xu Lin and Xinjian Lin Professor of Medicine Fujian Medical University ,
Adrenaline stimulates the proliferation and migration of mesenchymal stem cells towards the LPS-induced lung injury
Authors: Lingyan Wang
Chunxue Bai
Xiangdong Wang
Xiaodan Wu
Zhiming Wang
Mengjia Qian
Journal: Journal of Cellular and Molecular Medicine (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: acute lung injury; adrenergic receptor agonists; inflammation; lipopolysaccharide; mesenchymal stem cells.
Affiliations: Department of Pulmonary Medicine; Zhongshan Hospital; Fudan University; Shanghai China, Department of Medical Oncology; Zhongshan Hospital; Fudan University; Shanghai China, Biomedical Research Center; Zhongshan Hospital; Fudan University; Shanghai China

Abstract:  Bone marrow-derived mesenchymal stem cells (BMSCs) could modulate inflammation in experimental lung injury. On the other hand, adrenergic receptor agonists could increase DNA synthesis of stem cells. Therefore, we investigated the therapeutic role of adrenaline-stimulated BMSCs on lipopolysaccharide (LPS)-induced lung injury. BMSCs were cultured with adrenergic receptor agonists or antagonists. Suspensions of lung cells or sliced lung tissue from animals with or without LPS-induced injury were co-cultured with BMSCs. LPS-stimulated alveolar macrophages were co-cultured with BMSCs (with adrenaline stimulation or not) in Transwell for 6 hrs. A preliminary animal experiment was conducted to validate the findings in ex vivo study. We found that adrenaline at 10 μM enhanced proliferation of BMSCs through both α- and β-adrenergic receptors. Adrenaline promoted the migration of BMSCs towards LPS-injured lung cells or lung tissue. Adrenaline-stimulated BMSCs decreased the inflammation of LPS-stimulated macrophages, probably through the expression and secretion of several paracrine factors. Adrenaline reduced the extent of injury in LPS-injured rats. Our data indicate that adrenaline-stimulated BMSCs might contribute to the prevention from acute lung injury through the activation of adrenergic receptors, promotion of proliferation and migration towards injured lung, and modulation of inflammation. 

Retracted: No

PubPeer comments:
 Figure 4C: Migration images of different treatments show unexcepted similarity. ![file] ,
Transcriptional factors smad1 and smad9 act redundantly to mediate zebrafish ventral specification downstream of smad5
Authors: Yong-Hua Sun
Hou-Peng Wang
Chang-Yong Wei
Zuo-Yan Zhu
Journal: Journal of Biological Chemistry (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bone Morphogenetic Protein (BMP); Development; Dorso-ventral Patterning; Gene Regulation; Myelopoiesis
Affiliations: State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan 430072, China; University of the Chinese Academy of Sciences, Beijing 100049, China., State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan 430072, China., State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, 7 Donghu South Road, Wuhan 430072, China. Electronic address: .

Abstract:  Bone morphogenetic proteins (BMPs) are multifunctional growth factors that play crucial roles during embryonic development and cell fate determination. Nuclear transduction of BMP signals requires the receptor type Smad proteins, Smad1, Smad5, and Smad9. However, how these Smad proteins cooperate in vivo to regulate various developmental processes is largely unknown. In zebrafish, it was widely believed that the maternally expressed smad5 is essential for dorso-ventral (DV) patterning, and the zygotically transcribed smad1 is not required for normal DV axis establishment. In the present study, we have identified zygotically expressed smad9, which cooperates with smad1 downstream of smad5, to mediate zebrafish early DV patterning in a functional redundant manner. Although knockdown of smad1 or smad9 alone does not lead to visible dorsalization, double knockdown strongly dorsalizes zebrafish embryos, which cannot be efficiently rescued by smad5 overexpression, whereas the dorsalization induced by smad5 knockdown can be fully rescued by overexpression of smad1 or smad9. We have further revealed that the transcription initiations of smad1 and smad9 are repressed by each other, that they are direct transcriptional targets of Smad5, and that smad9, like smad1, is required for myelopoiesis. In conclusion, our study uncovers that smad1 and smad9 act redundantly to each other downstream of smad5 to mediate ventral specification and to regulate embryonic myelopoiesis. 

Retracted: No

PubPeer comments:
 2020 correction. https: www.jbc.org content 295 52 18650.short VOLUME 289 (2014) PAGES 6604u20136618 In Fig. 4G, in the foxi1 panel, the images in Fig. 4G, i and l, corresponding to u201csmad1 MOu201d and u201csmad5 MO + samd1 9 mRNAu201d samples, respectively, were inadvertently reused during figure preparation. This error has now been corrected using images pertaining to each treatment and sample. This correction does not affect the results or conclusions of the work. ,
Circulating Tumor Cells as a Biomarker to Assist Molecular Diagnosis for Early Stage Non-Small Cell Lung Cancer
Authors: Yutong He
Jin Shi
Bernd Schmidt
Zhaoyu Gao
Xiaoli Xu
Baoen Shan
Gaofeng Shi
Congmin Liu
Tiantian Guo
Qingyi Liu
Journal: Cancer management and research (2020)
Discipline: CLINICAL MEDICINE
Keywords: CellCollector; PD-L1; gene mutation; in vivo detection; next generation sequencing.
Affiliations: Cancer Institute, The Fourth Hospital of Hebei Medical University/The Tumor Hospital of Hebei Province, Shijiazhuang, Hebei 050011, People's Republic of China., Department of Internal Medicine - Pneumology and Sleep Medicine, Central Emergency Room, Palliative Medicine, DRK Kliniken Berlin, Berlin 13359, Germany., Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University/The Tumor Hospital of Hebei Province, Shijiazhuang, Hebei 050011, People's Republic of China., Department of Radiology, The Fourth Hospital of Hebei Medical University/The Tumor Hospital of Hebei Province, Shijiazhuang, Hebei 050011, People's Republic of China., Follow-Up Centre, The Fourth Hospital of Hebei Medical University/The Tumor Hospital of Hebei Province, Shijiazhuang, Hebei 050011, People's Republic of China.

Abstract:  Background and objective: Compared with tissue biopsy, liquid biopsy is the most preferable non-invasive promising method in personalized medicine, although it has many limitations in isolating circulating tumor cells (CTC). Lung cancer associated mortality is drastically increased due to a shortfall of early-stage detection, which remains a challenge. Herein, we aimed to detect lung cancer at an early-stage using CellCollector device. Methods: 39,627 volunteers underwent low-dose computed tomography; 2508 cases with pulmonary nodules and 7080 with no pulmonary nodules were chosen. After follow-up, 24 patients were diagnosed with early-stage non-small cell lung cancer (NSCLC), and subjected to CTC detection using CellCollector, along with 72 healthy volunteers. Immunofluorescence staining for EpCAM/CKs and CD45 were performed for CTC validation. Results: Fifteen out of twenty-four (stage I, n = 18; stage II, n = 6) early-stage lung cancer patients were found to be CTC-positive, whereas no CTC was found in the control group. Genetic mutation of TP53, ERBB2, PDGFRA, CFS1R and FGFR1 in the CTC revealed 71.6% of the mutation sites similar to the tumor tissues of 13 patients. Molecular characterization revealed higher expression of protein PD-LI in CTC (40%) as compared to tumor tissue (26.7%). Moreover, CTC clusters were detected in 40% of patients. Conclusion: CTC detection using the CellCollector in early-stage NSCLC had a relative high capture rate. Moreover, CTC analysis is a prospective setting for molecular diagnostic in cases when tumor tissue biopsy is not desirable. 

Retracted: No

PubPeer comments:
 In Figure 3, a microscopy panel has been duplicated and presented as something else. ![file] ,
Influence of lactic acid on the proliferation, metabolism, and differentiation of rabbit mesenchymal stem cells
Authors: Yan Zhou
Wen-Song Tan
Ting Chen
Journal: Cell Biology and Toxicology (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Lactic acid; rabbit mesenchymal stem cells; proliferation; metabolism; differentiation
Affiliations: State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, 200237, People's Republic of China.

Abstract:  Lactic acid, originated from degradation of biomaterials, cell cultures, and so on, would be a toxic compound in acute states. The present study was undertaken to ascertain whether the proliferation, metabolism, and differentiation of rabbit mesenchymal stem cells (rMSCs) were affected by additional lactic acid. Furthermore, this study aimed to determine whether this influence was due to decreasing pH, increasing osmotic pressure, or chemical action of lactate ion. It was shown that the proliferation and metabolism of MSCs were inhibited by decreasing pH or increasing lactate. However, when osmolarity was adjusted to the same level as that of sodium lactate using sodium chloride, cell proliferation was little affected by osmotic pressure. We also concluded that colony-forming potential and osteogenic differentiation capacity were significantly depressed by decreasing pH or increasing lactate. As was shown, this inhibition of lactate was not only due to osmotic pressure, but also mainly due to chemical action of lactate ion. However, we observed that acidifying extracellular medium and lactate ion promoted the retention of adipogenic differentiation potential of MSCs during in vitro expansion, which suggested that growth arrest and the decrease of osteogenic differentiation potential did not affect the adipogenic conversion of MSCs. 

Retracted: No

PubPeer comments:
 Fig 3C. Are these two control images meant to be the same? ![file] ,
RUNX2 RNA interference inhibits the invasion of osteosarcoma
Authors: Xiaotao Xu
Heng Zeng
Journal: Oncology letters (2015)
Discipline: CLINICAL MEDICINE
Keywords: RNA interference; RUNX2; invasion; osteocarsoma.
Affiliations: Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China., Department of Oncology, Renmin Hospital, Wuhan University, Wuhan, Hubei 430060, P.R. China.

Abstract:  It has previously been demonstrated that the expression of the RUNX2 gene is increased in osteosarcoma tissues or cell lines; however, there is little research available on the effect of RUNX2 on osteosarcoma invasion. In the present study, small interfering (si)RNA to RUNX2 was designed and synthesized, and then transfected into SAOS-2 cells. The effects of RUNX2 RNA interference on the invasion of osteosarcoma cells were detected by the soft agar colony forming test and Transwell® chamber assay. The expression of the associated proteins, vascular endothelial growth factor (VEGF), matrix metalloprotein-2 (MMP-2) and MMP-9, was detected by western blot analysis. The results revealed that the number of cell colonies was reduced dose-dependently by the siRNA and that the number of cells permeating through the filter membrane was decreased following transfection with the siRNA. The inhibition of RUNX2 caused a notable decrease in VEGF, MMP-2 and MMP-9 expression (0.16±0.04, 0.16±0.02 and 0.12±0.02) compared with the empty vector (0.86±0.22, 0.74±0.16 and 0.81±0.16) and blank control (0.78±0.12, 0.82±0.18 and 0.78±0.14) groups, respectively (P&lt;0.01). It can therefore be concluded that RUNX2 siRNA inhibits the invasion of osteosarcoma cells by inhibiting the expression of VEGF, MMP-2 and MMP-9. 

Retracted: No

PubPeer comments:
 This paper was found during a systematic search of papers in this journal with possible duplicated images. About 15% of the papers in this journal (n=98 examined) were found to contain inappropriately duplicated images. These papers have all been reported to the journal publisher in 2017. The editors promised to  investigate promptly but no action has been taken as of today. Figure 3. Panels  ConN and  ConB appear to show an area of overlap. Shown with red boxes. ![file] , 
 Figure 1 and Figure 5. Lanes 2-4 of the GAPDH panel in Figure 1 appear to look similar to lanes 1-3 of the GAPDH panel of Figure 5. The lanes represent different experiments. Shown with blue boxes. ![file] ,
MicroRNA-1246 enhances migration and invasion through CADM1 in hepatocellular carcinoma
Authors: Robert Chunhua Zhao
Qin Han
Chunmei Bai
Na Zhou
Shan Lu
Shihua Wang
Zhao Sun
Changting Meng
Mei Guan
Journal: BMC Cancer (2014)
Discipline: CLINICAL MEDICINE
Keywords: microRNAs; hepatocarcinoma; miR-1246; migration; invasion
Affiliations: Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, People's Republic of China. .

Abstract:  Background: The aberrant expression of microRNAs has been demonstrated to play a crucial role in the initiation and progression of hepatocarcinoma. miR-1246 expression in High invasive ability cell line than significantly higher than that in low invasive ability cell line. Methods: Transwell chambers (8-uM pore size; Costar) were used in the in vitro migration and invison anssay. Dual luciferase reporter gene construct and Dual luciferase reporter assay to identify the target of miR-1246. CADM1 expression was evaluated by immunohistochemistric staining. The clinical manifestations, treatments and survival were collected for statistical analysis. Results: Inhibition of miR-1246 effectively reduced migration and invasion of hepatocellular carcinoma cell lines. Bioinformatics and luciferase reporter assay revealed that miR-1246 specifically targeted the 3'-UTR of Cell adhesion molecule 1 and regulated its expression. Down-regulation of CADM1 enhanced migration and invasion of HCC cell lines. Furthermore, in tumor tissues obtained from liver cancer patients, the expression of miR-1246 was negatively correlated with CADM1 and the high expression of miR-1246 combined with low expression of CADM1 might serve as a risk factor for stage1 liver cancer patients. Conclusions: Our study showed that miR-1246, by down-regulation CADM1, enhances migration and invasion in HCC cells. 

Retracted: No

PubPeer comments:
 I realize splicing conventions have changed over time, but this looks more like a ransom note than a Western blot. TAM. *** Original ![file] *** Markup ![file] *** False color markup ![file] ,
Long non-coding RNA MNX1-AS1 promotes migration and invasion of esophageal squamous cell carcinoma by upregulating IGF2
Authors: C-J Zhang
D-N Zheng
G-P Sun
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Esophageal squamous cell carcinoma; long non-coding ribonucleic acids; MNX1-AS1; metastasis; mechanism
Affiliations: Department of Medical Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, China. .

Abstract:  Objective: Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor with a high mortality rate and poor prognosis. In this research, we investigated the exact role of long non-coding ribonucleic acids (lncRNA) MNX1-AS1 in the metastasis of ESCC and its possible mechanism. Patients and methods: To investigate the functions of MNX1-AS1 in ESCC, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect MNX1-AS1 expression of ESCC tissues and cells. Besides, functional assays, including transwell assay and wound healing assay, were performed. Furthermore, qRT-PCR and Western blot assay were used to explore the possible underlying regulatory mechanism. Results: The expression level of MNX1-AS1 was significantly increased in both ESCC tissues sample and cells. Moreover, knockdown of MNX1-AS1 markedly inhibited the migration and invasion of ESCC cells. Besides, knockdown of MNX1-AS1 remarkably down-regulated the mRNA and protein levels of insulin-like growth factor 2 (IGF2). Furthermore, IGF2 expression was positively correlated with MNX1-AS1 expression in ESCC tissues. Conclusions: MNX1-AS1 serves as a potential oncogene in ESCC, which can significantly promote ESCC cell migration and invasion by up-regulating IGF2. Our findings may provide a new therapeutic target of ESCC. 

Retracted: Yes

PubPeer comments:
 An article with the same title, same general structure, and very similar figures as been published in French by the same authors two years prior. There is no mention of this paper being a translation. Glevarec Hervu00e9, Cibois Philippe, u00ab Structure et historicitu00e9 des gou00fbts musicaux et cinu00e9matographiques. Analyse factorielle et interpru00e9tation sociologique u00bb, L Annu00e9e sociologique, 2018 2 (Vol. 68), p. 473-519. DOI : 10.3917 anso.182.0473. URL : https: www.cairn-int.info revue-l-annee-sociologique-2018-2-page-473.htm ,
LncRNA SPRY4-IT was concerned with the poor prognosis and contributed to the progression of thyroid cancer
Authors: Songwei Li
Haoyu Zhou
Xiaofeng Wang
Zhihua Sun
Xuejun Zhou
Journal: Cancer gene therapy (2018)
Discipline: CLINICAL MEDICINE
Keywords: lncRNAs; SPRY4-IT1; thyroid cancer; prognosis; TGF-β1
Affiliations: School of Food Science, Henan Institute of Science and Technology, Xinxiang, Henan Province, 453000, China., Institute of Tropical Agriculture and Forestry, Hainan University, Haikou, Hainan Province, 570228, China., School of resources and environment, Henan Institute of Science and Technology, Xinxiang, Henan Province, 453000, China., ENT & HN Surgery Department, The First Affiliated Hospital of Hainan Medical University, Haikou, Hainan Province, 570102, China. .

Abstract:  Long non-coding RNAs (lncRNAs) have been demonstrated to be critical regulators in tumorigenesis. LncRNA SPRY4-IT1 has been identified as critical regulator for hepatocellular carcinoma and ovarian cancer. However, the potential role and clinical value of SPRY4-IT1 in human thyroid cancer (TC) still remain unclear and need to be uncovered. Our current study was aimed to ascertain the biological role of expression of SPRY4-IT1 in TC tissues and cells. Our findings revealed that the level of SPRY4-IT1 was significantly upregulated in TC tissues and cell lines, which was correlated with poor prognosis. And cellular experiments exhibited that silenced SPRY4-IT1 inhibited the proliferative and migratory abilities of TC cells. Mechanism assays noted that silenced SPRY4-IT1 could increase the levels of transforming growth factor-β1 (TGF-β1) and p-Smad2/3 and function mediated by si-SPRY4-IT1 could be rescued by the interference of TGF-β1. Generally speaking, these findings elucidated that SPRY4-IT1 might become a novel prognostic factor in the clinical behaviors of TC patients and participated in the progression of TC through targeting TGF-β/Smad signaling pathway. 

Retracted: No

PubPeer comments:
 Another one from the list  The best of Cancer Gene Therapy 2018-2019 . Figure 3D is a falsification. In addition the Western blots are, let say, unusual. ![file] , 
 More than two years since I reported. No response from the authors and publisher. ,
Polyelectrolyte coated multilayered liposomes (nanocapsules) for the treatment of Helicobacter pylori infection
Authors: Sanyog Jain
Suresh P Vyas
Parul Jain
K N Prasad
S K Jain
Journal: Molecular pharmaceutics (0)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Helicobacter pylori; gastric cancers; drug delivery system; amoxicillin; metronidazole
Affiliations: Department of Pharmaceutical Sciences, Dr. Hari Singh Gour University, Sagar (M.P.) 470003, India., Department of Pharmaceutical Sciences, Dr. Hari Singh Gour University, Sagar (M.P.) 470003, India, Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research, Sector 67, SAS Nagar (Mohali), Punjab 160062, India, and Department of Microbiology, Sanjay Gandhi P.G. Institute of Medial Sciences, Lucknow (U.P.), India

Abstract:  Helicobacter pylori infection is one of the major causes of gastric cancers. A number of systems have already been reported, but 100% eradication has never been achieved. The present invention designs a gastro-retentive drug delivery system incorporated with amoxicillin and metronidazole, specifically suited for the eradication of Helicobacter pylori infections due to its mucoadhesiveness in the presence of polyelectrolyte polymers. The system possesses the advantages of both vesicular and particulate carriers, and it was prepared by alternative coating of polyanion (poly(acrylic acid), PAA) and polycation (poly(allylamine hydrochloride), PAH) using liposomes as the core. Compared with the conventional liposomes, the polyelectrolyte based multilayered system (nanocapsules) gave prolonged drug release in simulated gastric fluid, which is well suited for drug delivery against H. pylori infection in the stomach. In vitro growth inhibition study, agglutination assay, and in situ adherence assay in cultured H. pylori suggested the successful in vitro activity and binding propensity of the system. In vivo bacterial clearance study carried out in a H. pylori infected mouse model finally confirmed the success of the developed novel nanocapsule system. Thus, the newly developed composite nanocapsules along with the use of combination therapy proved to have commendable potential in Helicobacter pylori eradication as compared to already existing conventional and novel drug delivery systems. 

Retracted: No

PubPeer comments:
 Image recycling between two journals. ![file] ,
The correlation between microvessel pathological changes of the endplate and degeneration of the intervertebral disc in diabetic rats
Authors: Hao Peng
Jianping Li
Min Xiong
Meimei Liao
Sen Chen
Journal: Experimental and Therapeutic Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: diabetes mellitus; intervertebral disc; microvessel.

Abstract:  In this study, the pathological microvessel changes to the endplate and the degeneration of the intervertebral disc of diabetic rats were examined in order to identify the possible mechanism by which diabetes mellitus (DM) induces degeneration of the intervertebral disc. A total of 30 Sprague-Dawley rats were randomly divided into two groups. DM was induced in one of the groups by streptozotocin (STZ) administration. The rats were sacrificed 4, 8 and 12 weeks later. Five rats from each group were sacrificed at each time interval and lumbar disc and endplate tissue were obtained from each rat. The histological changes, collagen expression, microvessel density (MVD) and apoptosis of the disc were investigated by different methods. The expression of collagen I in the diabetic DM group was higher compared to the control group at the three time points (P&lt;0.01), in contrast to the expression of collagen II. The factor VIII-related antigen (FVIII RAg) was expressed in the control and DM groups, while its expression was relatively low in the DM group. The MVD of the DM group was smaller compared to that of the control group at the three time points (P&lt;0.01). The apoptotic index (AI) in the diabetic group was significantly higher compared to that of the control group at the three time points (P&lt;0.01). A negative correlation was observed between the MVD of the endplates and the notochordal cell AI in the two groups. Compared to the control group, the endplate MVD decreased and the cavity became smaller or disappeared in the diabetic rats. In conclusion, there was a negative correlation between MVD and degenerative changes of the intervertebral disc in diabetic rats. 

Retracted: Yes

PubPeer comments:
 Can the authors explain last part of Figure 2b? There is no description in the text. Three images of microtubes local grey value of holograms ? Why are the microtubes identical (three in the midle picture and all four in the picture to the right)? ![file] ,
Effect of Amoxicillin in combination with Imipenem-Relebactam against Mycobacterium abscessus
Authors: Jonathan A G Cox
Peter A Lambert
Rose C Lopeman
Daniel L Rathbone
Maya Desai
James Harrison
Journal: Scientific Reports (2020)
Discipline: Multidisciplinary
Keywords: Mycobacterium abscessus; cystic fibrosis; antibiotic resistance; therapeutic interventions; β-lactamase inhibitor
Affiliations: School of Life and Health Sciences, Aston University, Aston Triangle, B4 7ET, Birmingham, UK., Birmingham Children's Hospital, Birmingham Women's and Children's NHS Foundation Trust, Steelhouse Lane, B4 6NH, Birmingham, UK., School of Life and Health Sciences, Aston University, Aston Triangle, B4 7ET, Birmingham, UK. .

Abstract:  Infections caused by Mycobacterium abscessus are increasing in prevalence in cystic fibrosis patients. This opportunistic pathogen's intrinsic resistance to most antibiotics has perpetuated an urgent demand for new, more effective therapeutic interventions. Here we report a prospective advance in the treatment of M. abscessus infection; increasing the susceptibility of the organism to amoxicillin, by repurposing the β-lactamase inhibitor, relebactam, in combination with the front line M. abscessus drug imipenem. We establish by multiple in vitro methods that this combination works synergistically to inhibit M. abscessus. We also show the direct competitive inhibition of the M. abscessus β-lactamase, BlaMab, using a novel assay, which is validated kinetically using the nitrocefin reporter assay and in silico binding studies. Furthermore, we reverse the susceptibility by overexpressing BlaMab in M. abscessus, demonstrating relebactam-BlaMab target engagement. Finally, we highlight the in vitro efficacy of this combination against a panel of M. abscessus clinical isolates, revealing the therapeutic potential of the amoxicillin-imipenem-relebactam combination. 

Retracted: No

PubPeer comments:
 The value reported for k2 Ki (Relebactam BlaMab) in this publication is considerably higher than in two other recent publications. $2.32times10^6 M^{-1}s^{-1}$ vs. $6times10^2 M^{-1}s^{-1}$ https: aac.asm.org content early 2020 05 06 AAC.00098-20 $7.4times10^2 M^{-1}s^{-1}$ https: academic.oup.com jac article 75 2 379 5602193 The method section does not clearly describe how this value was obtained experimentally or the treatment of the obtained data. Could you please clarify: - How long was BlaMab incubated in the experiment described in Fig 2(b)? - Were the values for kobs (Fig 2(d)) obtained with or without preincubation? Best regards ,
LncRNA FBXL19-AS1 promotes proliferation and metastasis via regulating epithelial-mesenchymal transition in non-small cell lung cancer
Authors: Y-H Li
M Zhong
D-J Yu
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA; FBXL19-AS1; NSCLC; proliferation; metastasis
Affiliations: Department of Respiratory, China-Japan Union Hospital of Jilin University, Changchun, China. .

Abstract:  Objective: To detect the relative expression of long non-coding ribonucleic acid (lncRNA) F-box and leucine-rich repeat protein 19-antisense RNA 1 (FBXL19-AS1) in tissues and cells of non-small-cell lung cancer (NSCLC), and investigate the mechanism of lncRNA FBXL19-AS1 in promoting NSCLC cell proliferation and metastasis by regulating epithelial-mesenchymal transition (EMT) via in vitro experiments. Patients and methods: The relative expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells was detected via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The colony formation assay was performed to study the impact of interference with lncRNA FBXL19-AS1 expression on NSCLC cell proliferation. The flow cytometry was applied to determine the influence of si-FBXL19-AS1 on the cycle distribution of NSCLC cells. After the interference with lncRNA FBXL19-AS1 expression, the transwell assay was utilized to measure the changes in the migratory and invasive abilities of NSCLC cells, while the expression changes in EMT-related molecular markers was detected via Western blotting. Results: The results of qRT-PCR showed that the expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells was up-regulated. According to the results of the colony formation assay, the proliferative capacity of NSCLC cells was decreased after the interference with lncRNA FBXL19-AS1 expression. In flow cytometry, it was indicated that the cell cycle was arrested at the G0/G1 phase in the experimental group compared with that in the control group. The transwell assay results showed that the migratory and invasive abilities of NSCLC cells were weakened after the interference with lncRNA FBXL19-AS1 expression. The results of the Western blotting assay revealed that the expressions of EMT-related molecular markers (E-cadherin, N-cadherin, etc.) were changed. Conclusions: The expression of lncRNA FBXL19-AS1 in NSCLC tissues and cells is up-regulated, and the highly expressed lncRNA FBXL19-AS1 can promote NSCLC cell proliferation and metastasis by regulating the EMT. 

Retracted: No

PubPeer comments:
 Figure 3C. Several panels and several features within panels representing different treatments or cell lines appear to look similar to each other, albeit stretched differently or rotated. ![file] ,
Tool use changes multisensory interactions in seconds: evidence from the crossmodal congruency task
Authors: Gemma A Calvert
Charles Spence
Nicholas P Holmes
Journal: Experimental Brain Research (2007)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: tool use; neural representations; multisensory peripersonal space; crossmodal congruency effects; multisensory integration
Affiliations: Department of Experimental Psychology, University of Oxford, South Parks Road, Oxford OX1 3UD, UK. 

Abstract:  Active tool use in human and non-human primates has been claimed to alter the neural representations of multisensory peripersonal space. To date, most studies suggest that a short period of tool use leads to an expansion or elongation of these spatial representations, which lasts several minutes after the last tool use action. However, the possibility that multisensory interactions also change on a much shorter time scale following or preceding individual tool use movements has not yet been investigated. We measured crossmodal (visual-tactile) congruency effects as an index of multisensory integration during two tool use tasks. In the regular tool use task, the participants used one of two tools in a spatiotemporally predictable sequence after every fourth crossmodal congruency trial. In the random tool use task, the required timing and spatial location of the tool use task varied unpredictably. Multisensory integration effects increased as a function of the number of trials since tool use in the regular tool use group, but remained relatively constant in the random tool use group. The spatial distribution of these multisensory effects, however, was unaffected by tool use predictability, with significant spatial interactions found only near the hands and at the tips of the tools. These data suggest that endogenously preparing to use a tool enhances visual-tactile interactions near the tools. Such enhancements are likely due to the increased behavioural relevance of visual stimuli as each tool use action is prepared before execution. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: The two experiments in this paper had N=30 each, yet all our other similar papers 70471-4) had N=24. Why? We added 2x6 participants after checking the data because the important effects of interest were not significant. When N=30, the marginal p-values were .028 (spatial) and 0.046 (temporal). The conclusion from these numbers should therefore be that they are still not significant if you (Bonferroni) correct for the stopping-and-checking. The main problem, perhaps, is that I designed the study somewhat naively, requiring that a three-way interaction would be significant before interpreting the critical effects of interest. These borderline statistical results would not have mattered as much if we d been more specific about the critical comparisons in advance. ,