PReD-Bench/PRed-Bench huggingface dataset:
MicroRNA-140-5p inhibits invasion and angiogenesis through targeting VEGF-A in breast cancer
Authors: Q Zhang
L Wang
Y Lu
T Qin
J Mao
J Li
Z Jiang
Journal: Cancer Gene Therapy (2017)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-140-5p; breast cancer; invasion; angiogenesis
Affiliations: Teaching Laboratory of Morphology, Dalian Medical University, Dalian, China., Key Laboratory of Tumor Stem Cell Research of Liaoning Province, Dalian Medical University, Dalian, China., Department of Pathology, Dalian Medical University, Dalian, China.

Abstract:  MicroRNAs (miRNAs) have been proven to be involved in cell metastasis and angiogenesis by interaction with the target mRNAs. Evidence has been confirmed that miR-140-5p is a tumor suppressor in human cancers such as breast cancer. However, the potential molecular mechanism of miR-140-5p in breast cancer invasion and angiogenesis is still poorly understood. According to our study, we reported that miR-140-5p inhibited the tumor invasion and angiogenesis of breast cancer cells both in vitro and in vivo by targeting VEGF-A. The mRNA amount of miR-140-5p was decreased in the breast cancer clinical samples and breast cancer with metastasis compared with the corresponding adjacent normal tissues and cancer without metastasis. MiR-140-5p mimics and a negative control were transfected into human MCF-7 and MDA-MB-231 cells. Transwell chambers were used to detect the invasive ability of the cells, and the angiogenic ability was assessed by tube-formation assay. The markers of invasion and angiogenesis, VEGF-A, CD31 and MMP-9, were detected by using immunohistochemistry and western blot analysis in vivo. VEGF-A was verified as a possible target gene of miR-140-5p, and corroborated by dual-luciferase reporter and ELISA. Taken together, the study elucidates the molecular mechanisms by which miR-140-5p inhibits breast cancer metastasis and angiogenesis, and provides a potent evidence for the development of a novel microRNA-targeting anticancer strategy for breast cancer patients. 

Retracted: No

PubPeer comments:
 Figure 3c and d are falsified (three cases of data duplication and modification). The western immunoblot in Figure 5 is also suspicious (discontinuity; red arrow). ![file] , 
 There may also be some repeating features within these images. On close examination, it seems as if there are unexpected similarities and differences within and around these repeated features. *** ![file] , 
 #2 Similar issues with Figure 3b. One example marked. *** ![file] , 
 Erratum, [15 October 2020] . ------------------------------------------------------- The original version of this Article contained inaccuracies in Figs. 3 and 5. Figure 3: The authors apologize that due their neglect when doing the picture layout of Fig. 3c, the wrong transwell analysis image was pasted for Fig. 3d. The authors have replaced the wrong image. ![] Figure 5: The western blot for MMP-9 looks very unclear due to overexposure. Therefore, the authors rechecked the original data and images, and have replaced the problematic images with new ones. ![] The amendment to each figure does not affect the arguments or conclusion of the paper. ,
Two Mn(II)-Organic Frameworks: Selective Detection of Fe3+ Ion and Treatment Activity on Alcohol-Induced Cerebellar Atrophy By Reducing ROS Accumulation in Brain
Authors: Guan, En-Jie
Xia, Yan
Hu, Jian
Journal: Journal of Inorganic and Organometallic Polymers and Materials (2021)
Discipline: CHEMISTRY
Keywords: solvothermal reaction; Mn(II)-containing meta-organic frameworks (MOFs); mixed-ligand method; aromatic dicarboxylic acids; water stability

Abstract: Under solvothermal reaction conditions, two new Mn(II)-containing meta-organic frameworks (MOFs) having the chemical formula of [Mn(bda) (L)·0.5H2O]n (1) and [Mn(Hdda)2(L)·4H2O)]n (2) were prepared via a mixed-ligand method using different aromatic dicarboxylic acids ligands (H2bda\u2009=\u2009benzopheno-4,4-dicarboxylic acid, H2dda\u2009=\u20091,2-diethyl ether-4,4′-dibenzoic acid) and the flexible 1,3-di(1&nbsp;h-imidazol-1-yl)propane (L). Meanwhile, it is further demonstrated that complex 1 with excellent water stability can be used for a promising sensor for Fe3+ ions in aqueous solution, which has good selectivity and sensitivity. For the treatment of the alcohol-induced cerebellar atrophy, the accumulation of reactive oxygen species (ROS) in purkinje cells was evaluated by 2′,7′-dichlorofluorescin diacetate (DCFH-DA) assay. Besides, through real time reverse transcription-polymerase chain reaction (RT-PCR), the relative expression of ROS related gene in purkinje cells was detected.

Retracted: No

PubPeer comments:
 Could the authors clarify whether the materials described in [11] and [13] are indeed MOFs?  In addition, due to their the higher selectivity, the lower detection limit as well as excellent stability, the luminescent metal-organic frameworks (LMOFs) which is viewed as a chemical sensor for identifying biological-related molecules, explosive compounds, organic molecules and metal ions have drawn tremendous interests [10u201313] - [11]. D. Zhang, M.M. Wang, N. Jiang, Y. Liu, X.N. Yu, H.B. Zhang, Int. J. Electrochem. Sci. 15, 4117u20134126 (2020) ** Electrochemical Corrosion Behavior of Ni-doped ZnO Thin Film Coated on Low Carbon Steel Substrate in 3.5% NaCl Solution ** - [13]. J. Su, Z. Sheng, L. Xie, G. Li, IEEE Trans. Commun. 67, 2527u20132538 (2019) ** Fast Splitting Based Tag Identification Algorithm for Anti-Collision in UHF RFID System ** ,
LASS2 inhibits growth and invasion of bladder cancer by regulating ATPase activity
Authors: Ning Li
Jiansong Wang
Mingxia Ding
Changxing Ke
Wei Wang
Hui Zhan
Yigang Zuo
Haifeng Wang
Jingyu Liu
Ruping Yan
Journal: Oncology Letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: ATPase activity; bladder cancer; invasion and metastasis; longevity assurance homolog 2 of yeast LAG1.
Affiliations: Department of Urology, The Second Affiliated Hospital of Kunming Medical University, Yunnan Institute of Urology, Kunming, Yunnan 650101, P.R. China.

Abstract:  Homo sapiens longevity assurance homolog 2 of yeast LAG1 (LASS2) is a novel suppressor of human cancer metastasis, and downregulation of LASS2 has been associated with a poor prognosis in patients with bladder cancer (BC). However, the molecular mechanism underlying LASS2-mediated inhibition of tumor invasion and metastasis in BC remains unclear. LASS2 has been reported to directly bind to subunit C of vacuolar H+-ATPase (V-ATPase) in various types of cancer, suggesting that LASS2 may inhibit cancer invasion and metastasis by regulating the function of V-ATPase. The present study investigated the effect of LASS2-specific small interfering (si)RNA on the invasion and metastasis of the RT4 human BC cell line, which has a low metastatic potential, and its functional interaction with V-ATPase. Silencing of LASS2 in RT4 cells was able to increase V-ATPase activity, the extracellular hydrogen ion concentration and, in turn, the activation of secreted matrix metalloproteinase (MMP)-2 and MMP-9, which occurred simultaneously with enhanced cell proliferation, cell survival and cell invasion in vitro, as well as acceleration of BC growth in vivo. In this process, it was found that siRNA-LASS2 treatment was able to suppress cell apoptosis induced by doxorubicin. These findings suggest that silencing of LASS2 may enhance the growth, invasion and metastasis of BC by regulating ATPase activity. 

Retracted: No

PubPeer comments:
 Figure 2C appears to have a repeated image. (in different cell lines) ![file] , 
 Correction, [4 January 2022] . Subsequently to the publication of the above article, an interested reader drew to the authorsu2019 attention that the Matrigel invasion assays in Fig. 2C on p. 664 appeared to contain an error: Essentially, the T24 cell data were mistakenly selected twice for the siu2011LASS2 group, and also used to represent the RT4 experiment. However, the authors have consulted their original data, and have identified the correct data panel for the RT4 siu2011LASS2 experiment. The corrected version of Fig. 2, showing the correct data for Fig. 2C, is shown on the next page. Note that the errors in this figure did not affect either the results or the conclusions reported in this study. The authors are grateful to the Editor of *Oncology Letters* for granting them the opportunity to publish this corrigendum, and regret any inconvenience caused to the readership of the Journal. ,
The assessment of the optimal number of examined lymph nodes and prognostic models based on lymph nodes for predicting survival outcome in patients with stage N3b gastric cancer
Authors: Yue Wang
Muyan Shang
Zhe Dong
Shuai Guo
Yan Zhao
Jun Zhang
Journal: Asia-Pacific Journal of Clinical Oncology (2021)
Discipline: CLINICAL MEDICINE
Keywords: gastric adenocarcinoma; log odds of metastatic lymph nodes (LODDS); lymph node ratio (LNR); prognostic model; the optimal number of lymph node retrieved.
Affiliations: China Medical University  Shenbei New District Shenyang China, Department of Gastric Cancer Liaoning Cancer Hospital&amp; Institute (Cancer Hospital of China Medical University)  Shenyang China

Abstract:  Background: The optimal number of examined lymph nodes (ELNs) and the prognostic value of different nodal staging systems remain unclear in the context of N3b gastric cancer. Aim: To evaluate the optimal number of ELNs and compare the predictive ability of the ELN number, LN ratio (LNR), and log odds of metastatic LNs (LODDS) for overall survival (OS) in patients with resected stage N3b gastric adenocarcinoma in an international database. Methods: A total of 868 patients diagnosed between 2004 and 2015 in the Surveillance, Epidemiology, and End Results (SEER) database (training cohort) and 144 patients diagnosed between 2011 and 2016 at the Liaoning Cancer Hospital (validation cohort) were identified. Cutoff values were established with X-tile. The 5-year OS rates were compared using Kaplan-Meier curves. Multivariate analysis was conducted with a Cox regression model. The Harrell's concordance index and Akaike's information criterion were used to compare the predictive accuracy of different nodal staging systems. Results: The ELN number, LNR, and LODDS were independent prognostic factors for both the training and validation cohorts in the multivariate analysis. Patient with ≤26 ELNs, LNR of more than 0.9, and LODDS of more than 1.0 were associated with decrease OS. The LNR and LODDS had similar discriminatory ability for OS and performed better than the ELN number in the Eastern and Western populations. Conclusion: The optimal number of ELN may be 27 or more because LNs retrieved ≤26 was an independent risk factor for the prognosis. The prognostic prediction efficacy of LNR and LODDS was similar and better than that of ELN. Thus, LNR and LODDS could both serve as valid tools to predict OS for stage N3b patients. 

Retracted: No

PubPeer comments:
 The assessment of the optimal number of examined lymph nodes and prognostic models based on lymph nodes for predicting survival outcome in patients with stage N3b gastric cancer. ![file] The total number of Race in Table 1 is 552+113+202 =867, the percentage is 63.7+13.0+23.3=100%, and the Training set N=868, which is obviously wrong. ,
Robinin modulates TLR/NF-κB signaling pathway in oxidized LDL induced human peripheral blood mononuclear cells
Authors: Annie Abraham
P A Janeesh
C R Dhanya
V Sasikala
Journal: International Immunopharmacology (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Inflammatory marker enzymes; Oxidized LDL; Robinin; TLR-NF-κB signaling pathway; hPBMCs.
Affiliations: Department of Biochemistry, University of Kerala, Thiruvananthapuram, Kariavattom Campus, 695 581 Kerala, India., Department of Biochemistry, University of Kerala, Thiruvananthapuram, Kariavattom Campus, 695 581 Kerala, India. Electronic address: .

Abstract:  This study was designed to investigate whether robinin administration modulates toll-like receptor (TLR) and nuclear factor-kappa B (NF-κB) signaling pathway in oxidized LDL induced human peripheral blood mononuclear cells (hPBMCs). The hPBMCs were isolated from healthy human volunteers and the cells were cultured in collagen coated plates at 37°C with 5% CO2 and RPMI as culture medium and were grouped as follows: Group I - control, group II - OxLDL treated and group III - OxLDL+robinin (6μg/ml). We measured mRNA expression of TLR2 and TLR4 by reverse-transcriptase polymerase chain reaction (RT-PCR) and NF-κB transcription factor assay (ELISA), and western blotting studies were done for knowing expression of monocyte chemotactic protein-1 (MCP 1), tumor necrosis factor-alpha (TNF-α) interleukin-6 (IL-6) and vascular cell adhesion molecule 1 (VCAM-1). The result indicates that OxLDL that induces hPBMCs showed an upregulated expression of TLR2, TLR4, NF-κB, pro-inflammatory cytokines and VCAM-1. Robinin inhibited the ox-LDL induced TLR2 and TLR4 expression at mRNA level and inhibited the translocation of NF-κB p65 by modulating the TLR-NF-κB signaling pathway thereby inhibiting cytokine production and down regulated inflammatory enzymes like cyclooxygenase (COX), lipoxygenase (LOX), nitric oxide synthase (NOS) and prostaglandin E2 (PGE2), thus having protective effect against the ox-LDL induced inflammation stress in hPBMCs by inhibiting TLR4-NF-κB signaling pathway. 

Retracted: No

PubPeer comments:
 There are duplications in the histology images of Figure 5. We can look at the CA3 panels for controls and SCLM 140 mg kg. I have rotated the latter 180u00b0 for convenience: ![file] Interestingly. If we rotate them another 90u00b0 they match perfectly with an image used (multiple times) in a previous publication. Discussed separately here: https: pubpeer.com publications 3366DD20B5F81229F4DF6D446353CB ![file] Note that in that other publication, the image is associated with a whole different experimental treatment. The authors have quite a bit of explaining to do here. ,
Dexamethasone induces rapid serine-phosphorylation and membrane translocation of annexin 1 in a human folliculostellate cell line via a novel nongenomic mechanism involving the glucocorticoid receptor, protein kinase C, phosphatidylinositol 3-kinase, and mitogen-activated protein kinase
Authors: Roderick J Flower
Julia C Buckingham
Abeda Mulla
John F Morris
Egle Solito
Helen C Christian
Journal: Endocrinology (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: rat pituitary tissue; annexin 1; glucocorticoids; ACTH secretion; paracrine mechanism
Affiliations: Department of Neuroendocrinology (E.S., A.M., J.C.B.), Division of Neuroscience and Psychological Medicine, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, London W12 ONN, United Kingdom;, Human Anatomy and Genetics (J.F.M., H.C.C.), University of Oxford, Oxford OX1 3QX;, Department of Biochemical Pharmacology (R.J.F.), The William Harvey Research Institute, London EC1M 6BQ, United Kingdom

Abstract:  Our recent studies on rat pituitary tissue suggest that the annexin 1 (ANXA1)-dependent inhibitory actions of glucocorticoids on ACTH secretion are effected via a paracrine mechanism that involves protein kinase C (PKC)-dependent translocation of a serine-phosphorylated species of ANXA1 (Ser-P-ANXA1) to the plasma membrane of the nonsecretory folliculostellate cells. In the present study, we have used a human folliculostellate cell line (PDFS) to explore the signaling mechanisms that cause the translocation of Ser-P-ANXA1 to the membrane together with Western blot analysis and flow cytometry to detect the phosphorylated protein. Exposure of PDFS cells to dexamethasone caused time-dependent increases in the expression of ANXA1 mRNA and protein, which were first detected within 2 h of steroid contact. This genomic response was preceded by the appearance within 30 min of substantially increased amounts of Ser-P-ANXA1 and by translocation of the phosphorylated protein to the cell surface. The prompt membrane translocation of Ser-P-ANXA1 provoked by dexamethasone was inhibited by the glucocorticoid receptor, antagonist, mifepristone, but not by actinomycin D or cycloheximide, which effectively inhibit mRNA and protein synthesis respectively in our preparation. It was also inhibited by a nonselective PKC inhibitor (PKC(9-31)), by a selective inhibitor of Ca(2+)-dependent PKCs (Go 6976) and by annexin 5 (which sequesters PKC in other systems). In addition, blockade of phosphatidylinositiol 3-kinase (wortmannin) or MAPK pathways with PD 98059 or UO 126 (selective for MAPK kinse 1 and 2) prevented the steroid-induced translocation of Ser-P-ANXA1 to the cell surface. These results suggest that glucocorticoids induce rapid serine phosphorylation and membrane translocation of ANXA1 via a novel nongenomic, glucocorticoid receptor-dependent mechanism that requires MAPK, phosphatidylinositiol 3-kinase, and Ca(2+)-dependent PKC pathways. 

Retracted: No

PubPeer comments:
 Figures 4 and 5. Much more similar and different than expected. ![file] ,
Retracted : Upregulated microRNA‐31 inhibits oxidative stress‐induced neuronal injury through the JAK/STAT3 pathway by binding to PKD1 in mice with ischemic stroke
Authors: Jie Li
Yu-Qin Che
Hui Lv
Journal: Journal of Cellular Physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: JAK/STAT3 pathway; PKD1 gene; astrocytes; inflammatory response; ischemic stroke
Affiliations: Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, China.

Abstract:  Ischemic stroke (IS), which is characterized by high morbidity, disability, and mortality, is recognized as a major cerebrovascular disease. MicroRNA-31 (miR-31) was reported to participate in the progression of brain disease. The present study was conducted in order to investigate the effect of miR-31 on oxidative stress-induced neuronal injury in IS mice with the involvement of protein kinase D1 (PKD1) and the JAK/STAT3 pathway. C57BL/6J mice were used to establish the middle cerebral artery occlusion (MCAO) model. Astrocytes were transfected with miR-31 mimic, miR-31 inhibitor, si-PKD1, or JAK-STAT3 pathway inhibitor. Following the establishment of an oxygen-glucose deprivation (OGD) model, the astrocytes were cocultured with neuronal OGD. Lower miR-31, higher PKD1 expressions, and activated JAK/STAT3 pathway were found in both the MCAO and OGD models. miR-31 could negatively target PKD1. In an MCAO model, overexpressing miR-31 and silencing PKD1 reduced neuronal injury, cerebral infarct volume, neuron loss, and oxidative stress injury, inhibited the activation of JAK/STAT3 pathway and the expressions of PKD1, interleukin (IL)-1β, IL-6, tumor necrosis factor-α, malondialdehyde, 4-HNE, 8-HOdG, caspase-3, and Bax, but increased the superoxide dismutase content. In the OGD model, overexpression of miR-31 and silencing of PKD1 attenuated oxidative stress-induced neuronal injury, and diminished the lactate dehydrogenase leakage and reactive oxygen species level, accompanied by elevated neuronal viability. These results indicate that miR-31 alleviates inflammatory response as well as an oxidative stress-induced neuronal injury in IS mice by downregulating PKD1 and JAK/STAT3 pathway. 

Retracted: Yes

PubPeer comments:
 2021 retraction. https: onlinelibrary.wiley.com doi 10.1002 jcp.29773 u201cUpregulated microRNAu201031 inhibits oxidative stressu2010induced neuronal injury through the JAK STAT3 pathway by binding PKD1 in mice with ischemic strokeu201d from the Journal of Cellular Physiology, published online on 13 September 2019 in Wiley Online Library , and in Volume 235, pp. 2414u20132428, has been retracted by agreement between the journal s Editoru2010inu2010Chief, Gregg B. Fields, and John Wiley and Sons Ltd. The retraction follows an investigation which identified major flaws in the experimental design, leading to concerns about the validity of the results and the conclusions. The authors disagree with this decision. ,
Inhibition of processing of parathyroid hormone-related peptide by anti-sense furin: effect in vitro and in vivo on rat Leydig (H-500) tumor cells
Authors: N Amizuka
S A Rabbani
B Liu
D Goltzman
Journal: International Journal of Cancer (1995)
Discipline: CLINICAL MEDICINE
Keywords: Pro-parathyroid hormone-related peptide; Furin; PTHRP production; Adenylate cyclase-stimulating activity; Tumor cells
Affiliations: Department of Physiology, McGill University, Montreal, Canada.

Abstract:  To attain full biological activity, the precursor pro-parathyroid hormone-related peptide (ProPTHRP) must be converted to the mature peptide PTHRP. We have examined the effect of inhibiting expression of the pro-hormone convertase furin in H-500 rat Leydig tumor cells on PTHRP production and action in vitro and in vivo. H-500 Leydig tumor cells were stably transfected with a mammalian expression plasmid containing furin cDNA in an anti-sense orientation. This resulted in inhibition of endogenous furin mRNA expression and of protein production as assessed by immunocytochemistry. These experimental cells secreted extended NH2-terminal PTHRP forms with reduced adenylate cyclase-stimulating activity. This was associated with a marked decrease in the proliferation of these tumor cells in vitro. Transfected and control cells were then implanted into male Fischer rats. Animals implanted with control cells became hypercalcemic. In contrast, animals implanted with experimental cells maintained near normal levels of plasma calcium. Experimental cells inoculated in vivo developed into tumors of significantly decreased volume compared to control cells and animal survival time was prolonged. Our results indicate that alteration of the processing of PTHRP can diminish the hypercalcemic endocrine actions of PTHRP and can reduce autocrine/paracrine effects of PTHRP on tumor cell growth both in vitro and in vivo. Furin may also exert a broader role in processing other factors required for tumor proliferation. Consequently, anti-sense modulation of furin activity may be a potential modality for understanding the mechanism of neoplastic growth and progression. 

Retracted: No

PubPeer comments:
 Figure 1. Furin antisense panel. Lanes 1 and 2 have different background from lane 3. ![file] ,
Regulation of Cigarette Smoke (CS)-Induced Autophagy by Nrf2
Authors: Aditya Manoharan
Lingxiang Zhu
Yuxue Xu
Yin Chen
Erika C Barrett
Zuguo Liu
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Cigarette smoke; autophagy; COPD; LC3B; Nrf2
Affiliations: Department of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona, United States of America.

Abstract:  Cigarette smoke (CS) has been reported to induce autophagy in airway epithelial cells. The subsequent autophagic cell death has been proposed to play an important pathogenic role in chronic obstructive pulmonary disease (COPD); however, the underlying molecular mechanism is not entirely clear. Using CS extract (CSE) as a surrogate for CS, we found that it markedly increased the expressions of both LC3B-I and LC3B-II as well as autophagosomes in airway epithelial cells. This is in contrast to the common autophagy inducer (i.e., starvation) that increases LC3B-II but reduces LC3B-I. Further studies indicate that CSE regulated LC3B at transcriptional and post-translational levels. In addition, CSE, but not starvation, activated Nrf2-mediated adaptive response. Increase of cellular Nrf2 by either Nrf2 overexpression or the knockdown of Keap1 (an Nrf2 inhibitor) significantly repressed CSE-induced LC3B-I and II as well as autophagosomes. Supplement of NAC (a GSH precursor) or GSH recapitulated the effect of Nrf2, suggesting the increase of cellular GSH level is responsible for Nrf2 effect on LC3B and autophagosome. Interestingly, neither Nrf2 activation nor GSH supplement could restore the repressed activities of mTOR or its downstream effctor-S6K. Thus, the Nrf2-dependent autophagy-suppression was not due to the re-activation of mTOR-the master repressor of autophagy. To search for the downstream effector of Nrf2 on LC3B and autophagosome, we tested Nrf2-dependent genes (i.e., NQO1 and P62) that are also increased by CSE treatment. We found that P62, but not NQO1, could mimic the effect of Nrf2 activation by repressing LC3B expression. Thus, Nrf2-&gt;P62 appears to play an important role in the regulation of CSE-induced LC3B and autophagosome. 

Retracted: No

PubPeer comments:
 January 2014 correction for a mis-spelled name. Some issues in Figure 5 reported in 2015 have not been addressed, however. Figure 5. * Blue arrows: Sharp vertical background transitions appear to be visible * Red ellipses: In Figure 5A, two lanes in the actin panel appear to look similar * Purple ellipses: In Figure 5B, two lanes in the actin panel appear to look similar * Green ellipses: In Figure 5C, lanes 5-6 in the actin panel appear to look similar to lanes 7-8. ![file] , 
 Figure 2D. * Red arrows: In the LC3 panel, lane 1 looks like the mirror image of lane 2 * Blue arrows: In the Actin panel, lanes 4-5 look like the mirror image of lanes 7-8. ![file] , 
 Figure 3B. * Some lanes look more similar than expected. Arrows of the same color highlight similarities and respective orientation between lanes that represent different experiments. ![file] ,
Hepatocyte growth factor differently influences Met-E-cadherin phosphorylation and downstream signaling pathway in two models of breast cells
Authors: E Ridolfi
E Matteucci
M A Desiderio
Journal: Cellular and Molecular Life Sciences (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: E-cadherins; cell adhesion; cell signaling; tyrosine kinase-receptors; Met
Affiliations: Institute of General Pathology, University of Milan, via Luigi Mangiagalli 31, 20133 Milan, Italy.

Abstract:  E-cadherins are implicated in cell adhesion, and also in cell signaling by associating with tyrosine kinase-receptors such as Met, the hepatocyte growth factor (HGF) receptor. Using two different cellular models, i.e. MCF-7 (breast carcinoma) and MCF-10 (immortalized mammary) cells, we studied the possible mechanism(s) by which E-cadherins modulate the signaling pathways downstream of Met, leading to beta-catenin-TCF transcriptional activity. In MCF-7, but not in MCF-10 cells, E-cadherins were remarkably associated with Met. Moreover, in MCF-7 cells both co-immunoprecipitation with anti-Met antibody and co-localization were increased by 30-min HGF treatment, which caused E-cadherin tyrosine phosphorylation. Also beta-catenin in the co-immunoprecipitate was phosphorylated by HGF, probably favoring TCF activation. Consistently, after HGF treatment, beta-catenin redistributed earlier in MCF-7 than in MCF-10 cells, with nuclear accumulation and activation of TOPFLASH gene reporter. Our results indicate a functional role of Met-E-cadherin interaction in MCF-7 cells through the amplification of the signaling downstream of HGF-Met triggering that involved c-Src and phosphoinositide-3-kinase activities. 

Retracted: No

PubPeer comments:
 #1 For 5C,E Br J Cancer 99 and 1b Cell Mol Life Sci 63 it looks like an inattention in the graphical assembling of the acquisitions, since the aspect of the vinculins is very similar. A Phd who does not work any more in the group prepared these Figures. , 
null, 
 Fig 1(a) at *[left]* . Compared with *[right]* Fig 3A from [Ridolfi et al (2008)] . ![file] Could the authors clarify whether the lanes run from left to right, or vice versa? And which cell lines they derive from? ,
Constitutive activation of GSK3 down-regulates glycogen synthase abundance and glycogen deposition in rat skeletal muscle cells
Authors: Anne S Blair
Otto Baba
Harinder S Hundal
Calum Sutherland
Tatsuo Terashima
Katrina MacAulay
Eric Hajduch
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: GSK3; glycogen synthase; GS protein; muscle cells; differentiation

Abstract:  The effects of inhibition or constitutive activation of glycogen synthase kinase-3 (GSK3) on glycogen synthase (GS) activity, abundance, and glycogen deposition in L6 rat skeletal muscle cells were investigated. GS protein expression increased approximately 5-fold during differentiation of L6 cells (comparing cells at the end of day 5 with those at the beginning of day 3). However, exposure of undifferentiated myoblasts (day 3) to 50 microM SB-415286, a GSK3 inhibitor, led to a significant elevation in GS protein that was not accompanied by changes in the abundance of GLUT4, another late differentiation marker. In contrast, stable expression of a constitutively active form of GSK3beta (GSK3S9A) led to a significant reduction (approximately 80%) in GS protein that was antagonized by SB-415286. Inhibition of GSK3 or expression of the constitutively active GSK3S9A did not result in any detectable changes in GS mRNA abundance. However, the increase in GS protein in undifferentiated myoblasts or that seen following incubation of cells expressing GSK3S9A with GSK3 inhibitors was blocked by cycloheximide suggesting that GSK3 influences GS abundance possibly via control of mRNA translation. Consistent with the reduction in GS protein, cells expressing GSK3S9A were severely glycogen depleted as judged using a specific glycogen-staining antibody. Inhibiting GSK3 in wild-type or GSK3S9A-expressing cells using SB-415286 resulted in an attendant activation of GS, but not that of glucose transport. However, GS activation alone was insufficient for stimulating glycogen deposition. Only when muscle cells were incubated simultaneously with insulin and SB-415286 or with lithium (which stimulates GS and glucose transport) was an increase in glycogen accretion observed. Our findings suggest that GSK3 activity is an important determinant of GS protein expression and that while glycogen deposition in muscle cells is inherently dependent upon the activity/expression of GS, glucose transport is a key rate-determining step in this process. 

Retracted: No

PubPeer comments:
 Figure 3B. Much more similar than expected. ![file] ,
WIP regulates N-WASP-mediated actin polymerization and filopodium formation
Authors: J H Hartwig
R Rohatgi
M Medina
N Martinez-Quiles
S P Saville
T Takenawa
H Miki
R S Geha
N Ramesh
H Yamaguchi
I M Antón
Journal: Nature Cell Biology (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: filopodia; Cdc42; N-WASP; WIP; actin
Affiliations: Department of Pediatrics, Division of Immunology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Abstract:  Induction of filopodia is dependent on activation of the small GTPase Cdc42 and on neural Wiskott-Aldrich-syndrome protein (N-WASP). Here we show that WASP-interacting protein (WIP) interacts directly with N-WASP and actin. WIP retards N-WASP/Cdc42-activated actin polymerization mediated by the Arp2/3 complex, and stabilizes actin filaments. Microinjection of WIP into NIH 3T3 fibroblasts induces filopodia; this is inhibited by microinjection of anti-N-WASP antibody. Microinjection of anti-WIP antibody inhibits induction of filopodia by bradykinin, by an active Cdc42 mutant (Cdc42(V12)) and by N-WASP. Our results indicate that WIP and N-WASP may act as a functional unit in filopodium formation, which is consistent with their role in actin-tail formation in cells infected with vaccinia virus or Shigella. 

Retracted: No

PubPeer comments:
 Figure 1a. Much more similar than expected. ![file] , 
 #1 * Much more similar than expected * Disagree. These are not even *slightly* more similar than expected; instead, they are within the range of expected similarity. Furthermore, they contain several distinguishing features; in particular, the patterns of intensity above and below the darkest row of pixels is different in the two bands. Not worth further consideration. A zoomed-in view of the ROI: ![file] , 
 Thank you for bringing this to attention I concur with the above ,
Biphasic effects of TGFβ1 on BMP9-induced osteogenic differentiation of mesenchymal stem cells
Authors: Xiaoji Luo
Liangjun Yin
Zhong-Liang Deng
Jinyong Luo
Xi Liang
Tong-Chuan He
Wei Shui
Liang Chen
Bo Liu
Ning Hu
Rui-Dong Li
Wei Huang
Journal: BMB Reports (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: BMP9; TGFβ1; osteogenic differentiation; alkaline phosphatase activity; matrix mineralization
Affiliations: Department of Orthopaedic Surgery, the First Affiliated Hospital, Chongqing Medical University, Chongqing, China.

Abstract:  We have found that the previously uncharacterized bone morphogenetic protein-9 (BMP9) is one of the most osteogenic factors. However, it is unclear if BMP9 cross-talks with TGFβ1 during osteogenic differentiation. Using the recombinant BMP9 adenovirus, we find that low concentration of rhTGFβ1 synergistically induces alkaline phosphatase activity in BMP9-transduced C3H10T1/2 cells and produces more pronounced matrix mineralization. However, higher concentrations of TGFβ1 inhibit BMP9-induced osteogenic activity. Real-time PCR and Western blotting indicate that BMP9 in combination with low dose of TGFβ1 potentiates the expression of later osteogenic markers osteopontin, osteocalcin and collagen type 1 (COL1a2), while higher concentrations of TGFβ1 decrease the expression of osteopontin and osteocalcin but not COL1a2. Cell cycle analysis reveals that TGFβ1 inhibits C3H10T1/2 proliferation in BMP9-induced osteogenesis and restricts the cells in G(0)/G(1) phase. Our findings strongly suggest that TGFβ1 may exert a biphasic effect on BMP9-induced osteogenic differentiation of mesenchymal stem cells. 

Retracted: No

PubPeer comments:
 Figure 2 * Green boxes: Two panels appear to look more similar than expected * Pink boxes: Two panels appear to show an overlap ![file] , 
 #1 Thanks for identifying these potential errors. We are examining our original image files and will address them shortly. , 
 It has recently come to our attention that there was an image assembling error for Figure 2. Specifically, the image for u201cGFP-Day13u201d group was inadvertently duplicated from that for u201cBT20-Day 5u201d group, and an incorrect image was used for u201cGFP-Day 17u201d group. The corrected Figure 2 is shown as the following image. All authors were aware of the errors and approved the corrected figure. Even though the mistake did not affect the overall conclusion of our study, we apologize for any inconvenience caused to the readers and the scientific community. ![file] ,
Efficient wettability-controlled electroreduction of CO2 to CO at Au/C interfaces
Authors: Xuerui Zhang
Lei Jiang
Geoffrey I N Waterhouse
Lu Shang
Zhaojun Han
Yunxuan Zhao
Chao Zhou
Run Shi
Jiahao Guo
Tierui Zhang
Journal: Nature Communications (2020)
Discipline: Multidisciplinary
Keywords: electrochemical CO2 reduction reaction; electrocatalyst design; wettability-controlled interfacial structures; gas-liquid-solid interfaces; Au/C gas diffusion electrode
Affiliations: Key Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing, 100190, China., Center of Materials Science and Optoelectronics Engineering, University of Chinese Academy of Sciences, Beijing, 100049, China., School of Chemical Sciences, The University of Auckland, Auckland, 1142, New Zealand., CSIRO Manufacturing, New South Wales, 2070, Australia., Key Laboratory of Bio-inspired Materials and Interfacial Science, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing, 100190, China., Key Laboratory of Photochemical Conversion and Optoelectronic Materials, Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing, 100190, China. ., Center of Materials Science and Optoelectronics Engineering, University of Chinese Academy of Sciences, Beijing, 100049, China. .

Abstract:  The electrochemical CO2 reduction reaction (CO2RR) represents a very promising future strategy for synthesizing carbon-containing chemicals in a more sustainable way. In spite of great progress in electrocatalyst design over the last decade, the critical role of wettability-controlled interfacial structures for CO2RR remains largely unexplored. Here, we systematically modify the structure of gas-liquid-solid interfaces over a typical Au/C gas diffusion electrode through wettability modification to reveal its contribution to interfacial CO2 transportation and electroreduction. Based on confocal laser scanning microscopy measurements, the Cassie-Wenzel coexistence state is demonstrated to be the ideal three phase structure for continuous CO2 supply from gas phase to Au active sites at high current densities. The pivotal role of interfacial structure for the stabilization of the interfacial CO2 concentration during CO2RR is quantitatively analysed through a newly-developed in-situ fluorescence electrochemical spectroscopic method, pinpointing the necessary CO2 mass transfer conditions for CO2RR operation at high current densities. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Cholesteryl oleate-loaded cationic solid lipid nanoparticles as carriers for efficient gene-silencing therapy
Authors: Josep Mª Suñé-Negre
Silvia Prieto-Sánchez
Younes El Yousfi
Cristina Hernández-Munain
Josep Ramón Ticó
Marc Suñé-Pou
Isaac Nofrerias-Roig
Sofía Boyero-Corral
Carlos Suñé
Pilar Pérez-Lozano
Anna Nardi-Ricart
Encarna García-Montoya
Montserrat Miñarro-Carmona
Journal: International Journal of Nanomedicine (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: SLNs; cationic solid lipid nanoparticles; cholesteryl oleate; cytotoxicity; plasmid DNA
Affiliations: Service of Development of Medicines (SDM), Faculty of Pharmacy, University of Barcelona, Barcelona, Spain., Department of Molecular Biology, Institute of Parasitology and Biomedicine "López-Neyra" (IPBLN-CSIC), Granada, Spain., Pharmacotherapy, Pharmacogenetics and Pharmaceutical Technology Research Group, IDIBELL-UB, Duran i Reynals Hospital, Hospitalet de Llobregat, Barcelona, Spain., Department of Cell Biology and Immunology, Institute of Parasitology and Biomedicine "López-Neyra" (IPBLN-CSIC), Granada, Spain.

Abstract:  Background: Cationic solid lipid nanoparticles (SLNs) have been given considerable attention for therapeutic nucleic acid delivery owing to their advantages over viral and other nanoparticle delivery systems. However, poor delivery efficiency and complex formulations hinder the clinical translation of SLNs. Aim: The aim of this study was to formulate and characterize SLNs incorporating the cholesterol derivative cholesteryl oleate to produce SLN-nucleic acid complexes with reduced cytotoxicity and more efficient cellular uptake. Methods: Five cholesteryl oleate-containing formulations were prepared. Laser diffraction and laser Doppler microelectrophoresis were used to evaluate particle size and zeta potential, respectively. Nanoparticle morphology was analyzed using electron microscopy. Cytotoxicity and cellular uptake of lipoplexes were evaluated using flow cytometry and fluorescence microscopy. The gene inhibition capacity of the lipoplexes was assessed using siRNAs to block constitutive luciferase expression. Results: We obtained nanoparticles with a mean diameter of approximately 150-200 nm in size and zeta potential values of 25-40 mV. SLN formulations with intermediate concentrations of cholesteryl oleate exhibited good stability and spherical structures with no aggregation. No cell toxicity of any reference SLN was observed. Finally, cellular uptake experiments with DNA-and RNA-SLNs were performed to select one reference with superior transient transfection efficiency that significantly decreased gene activity upon siRNA complexation. Conclusion: The results indicate that cholesteryl oleate-loaded SLNs are a safe and effective platform for nonviral nucleic acid delivery. 

Retracted: No

PubPeer comments:
 u201cEditor who approved publication: Prof. Dr. Thomas J Websteru201d https: imgur.com a Q9uJybp ,
Curcumol Suppresses Breast Cancer Cell Metastasis by Inhibiting MMP-9 Via JNK1/2 and Akt-Dependent NF-κB Signaling Pathways
Authors: Qianfeng Chen
Ling Ning
Hongyi Qi
Hui Ma
Zhuyun Jiang
Lu Chen
Li Li
Journal: Integrative cancer therapies (2016)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Akt; MAPK; MMP-9; NF-κB; breast cancer metastasis
Affiliations: Southwest University, Chongqing, China., Southwest University, Chongqing, China .

Abstract:  Curcumolhas been reported to possess antitumor activity. However, its effect and mechanisms against tumor metastasis are still unclear. This study is to investigate the inhibitory effect of curcumol on breast cancer cell metastasis and elucidate the underlying molecular mechanisms. Our results showed that noncytotoxicity was caused by curcumol within 10 to 40 µg/mL in MDA-MB-231 and 4T1 cells for 24 hours, whereas sustained treatment with curcumol for 14 days significantly suppressed the clonogenic activity of cells. Importantly, curcumol at noncytotoxic concentrations suppressed the migration ability of both MDA-MB-231 and 4T1 cells. Moreover, curcumol suppressed the migration and invasion of MDA-MB-231 cells in the Boyden chamber migration and invasion assay and inhibited the adhesion of MDA-MB-231 cells onto the matrigel. Further investigations revealed that curcumol decreased the enzyme activity and protein expression of matrix metalloproteinase (MMP-9) in MDA-MB-231 cells. Moreover, curcumol inhibited the activation of c-Jun N-terminal kinase (JNK) 1/2 and Akt (Ser473). Meanwhile, it also inhibited the nuclear translocation and transcriptional activity of nuclear factor κB (NF-κB). Furthermore, JNK inhibitor SP600125 and Akt (Ser473) inhibitor LY294002 enhanced the inhibition of curcumol on NF-κB p65 nuclear translocation. Finally, supplementation with SP600125, LY294002, or NF-κB inhibitor Ammonium pyrrolidinedithiocarbamate (PDTC) significantly enhanced the inhibitory effect of curcumol on MMP-9 expression and cell migration, invasion, and adhesion in MDA-MB-231 cells. Our findings provide evidence for the suppression of breast cancer cell metastasis by curcumol and suggest that the inhibition of MMP-9 via JNK1/2 and Akt (Ser473)-dependent NF-κB signaling pathways may be the underlying mechanisms. 

Retracted: No

PubPeer comments:
 Figure 6 seems peculiarly unclear about its purpose. Forensically found more, but I will leave that effort to other readers. *** ![file] *** ![file] *** Full figure ![file] *** ![file] , 
 Fig 3D: ![file] , 
 #1 I am impressed how well Foresically performed on 6D. ![file] Fig 3B C and Fig 6B C: ![file] ,
Increased osteoblast adhesion on nanoparticulate crystalline hydroxyapatite functionalized with KRSR
Authors: Michael Nelson
Ganesan Balasundaram
Thomas J Webster
Journal: International Journal of Nanomedicine (2006)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: nanometer crystalline hydroxyapatite; amorphous calcium phosphate; orthopedic applications; nanoparticles; wet chemical process
Affiliations: Department of Chemical Engineering, Michigan State University, East Lansing, MI, USA.

Abstract:  The present in vitro study created nanometer crystalline hydroxyapatite (HA) and amorphous calcium phosphate for novel orthopedic applications. Specifically, nano-crystalline HA and amorphous calcium phosphate nanoparticles were synthesized by a wet chemical process followed by hydrothermal treatment for 2 hours at 200 degrees C and 70 degrees C, respectively. Resulting particles were then pressed into compacts. For the preparation of control conventional HA particles (or those currently used in orthopedics with micron diameters), the aforementioned calcium phosphate particles were pressed into compacts and sintered at 1100 degrees C for 2 hours. All calcium phosphate-based particles were fully characterized. Results showed that although there was an initial weight gain for all the compacts studied in this experiment, higher eventual degradation rates up to 3 weeks were observed for nano-amorphous calcium phosphate compared with nano-crystalline HA which was higher than conventional HA. Peptide functionalization (with the cell adhesive peptide lysine-arginine-serine-arginine [KRSR] and the non-cell-adhesive peptide lysine-serine-arginine-arginine [KSRR]) was accomplished by means of a three-step reaction procedure: silanization with 3-aminopropyltriethoxysilane (APTES), cross-linking with N-succinimidyl-3-maleimido propionate (SMP), and finally peptide immobilization. The peptide functionalization was fully characterized. Results demonstrated increased osteoblast (bone-forming cell) adhesion on non-functionalized and functionalized nano-crystalline HA compacts compared with nano amorphous calcium phosphate compacts; both increased osteoblast adhesion compared with conventional HA. To further exemplify the novel properties of nano crystalline HA, results also showed similar osteoblast adhesion between non-functionalized nano crystalline HA and KRSR functionalized conventional HA. Thus, results provided evidence that nanocrystalline HA should be further studied for orthopedic applications. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: Panels a1 and a2 appear to look very similar. Could the authors please clarify if these are showing the same measurements, please? ![file] ,