PReD-Bench/PRed-Bench huggingface dataset:
Quick Microwave Assisted Synthesis and In Vitro Imaging Application of Oxygen Doped Fluorescent Carbon Dots
Authors: Raja Angamuthu
Ramesh Rajendran
Raj Vairamuthu
Journal: Journal of fluorescence (2018)
Discipline: CHEMISTRY
Keywords: Fluorescent carbon dots; Microwave synthesis; Surface morphology, Cytotoxicity and in vitro imaging.
Affiliations: Advanced Materials Research Laboratory, Department of Chemistry, Periyar University, Salem, Tamil Nadu, 636 011, India., Energy and Functional Materials Laboratory, Department of Physics, Periyar University, Salem, Tamil Nadu, 636 011, India., Advanced Materials Research Laboratory, Department of Chemistry, Periyar University, Salem, Tamil Nadu, 636 011, India. ., Centre for Nanoscience and Nanotechnology, Periyar University, Salem, Tamil Nadu, 636 011, India. .

Abstract:  In this paper, a fast and simplest one-pot tactic was used to synthesis fluorescent oxygen doped carbon dots from Tween-20 (TTO-CDs) is reported. The TTO-CDs were microwavically synthesized by using Tween-20 as both the carbon precursor and the oxygen dopant as well. The surface morphology, crystalline and/or amorphous nature, composition and optical assets of synthesized TTO-CDs were studied by means of existing techniques. From the results, it was confirmed that the as-synthesized TTO-CDs are amorphous in nature, monodispersed, sphere-shaped and the typical particle size range is 5 ± 1.5 nm. The synthesized TTO-CDs emits strong blue fluorescence at 390 nm under excitation of 335 nm. Most interestingly, the excitation dependent emission property of synthesized TTO-CDs was exposed from fluorescence results. The synthesized TTO-CDs have quantum yield of about 14% against quinine sulfate as reference standard. The biotoxicity of synthesized TTO-CDs on HeLa cells was assessed through cytotoxicity assay. These results implied that the fluorescent TTO-CDs showed less biotoxicity, and further which was efficaciously applied as a multicolor staining and bioimaging probe for the confocal imaging of HeLa cells. 

Retracted: No

PubPeer comments:
 ![file] , 
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 Fig 7  Confocal microscopy images of HeLa cells treated with 20 u03bcg mLu22121 of the TTO-CDs. (a) blue (465u2013486), (b) green (508u2013540), (c) yellow (561u2013 604) (d) red (636u2013700) excited at wavelength 488 nm; (e) bright field and (f) merged confocal images . The Figure has had an eventful career. Here, at right, rotated, compared with Fig 10 from [Gomathi Asaithambi et al (2018)] : ![] Here, unrotated, compared with (left) 90-deg-rotated Fig 11 from [Gomathi Asaithambi et al (2019)] . ![] Here, compared with (above) Fig 12 from [Asaithambi Gomathi et al (2019)] : ![] I should add that it is really up to the authors of those other three papers to explain the re-use of the image, as they were published *after* this paper. No reflection on the present authors is intended. ,
PPAR-γ activation increases insulin secretion through the up-regulation of the free fatty acid receptor GPR40 in pancreatic β-cells
Authors: Kyong Soo Park
Kwang-Won Kim
Myung-Shik Lee
Hyo-Sup Kim
Moon-Kyu Lee
Seung-Hoi Koo
You-Cheol Hwang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: PPAR-γ activation; insulin secretion; GPR40; intracellular calcium mobilization; IRS-2
Affiliations: Division of Endocrinology and Metabolism, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea.

Abstract:  Background: It has been reported that peroxisome proliferator-activated receptor (PPAR)-γ and their synthetic ligands have direct effects on pancreatic β-cells. We investigated whether PPAR-γ activation stimulates insulin secretion through the up-regulation of GPR40 in pancreatic β-cells. Methods: Rat insulinoma INS-1 cells and primary rat islets were treated with rosiglitazone (RGZ) and/or adenoviral PPAR-γ overexpression. OLETF rats were treated with RGZ. Results: PPAR-γ activation with RGZ and/or adenoviral PPAR-γ overexpression increased free fatty acid (FFA) receptor GPR40 expression, and increased insulin secretion and intracellular calcium mobilization, and was blocked by the PLC inhibitors, GPR40 RNA interference, and GLUT2 RNA interference. As a downstream signaling pathway of intracellular calcium mobilization, the phosphorylated levels of CaMKII and CREB, and the downstream IRS-2 and phospho-Akt were significantly increased. Despite of insulin receptor RNA interference, the levels of IRS-2 and phospho-Akt was still maintained with PPAR-γ activation. In addition, the β-cell specific gene expression, including Pdx-1 and FoxA2, increased in a GPR40- and GLUT2-dependent manner. The levels of GPR40, phosphorylated CaMKII and CREB, and β-cell specific genes induced by RGZ were blocked by GW9662, a PPAR-γ antagonist. Finally, PPAR-γ activation up-regulated β-cell gene expressions through FoxO1 nuclear exclusion, independent of the insulin signaling pathway. Based on immunohistochemical staining, the GLUT2, IRS-2, Pdx-1, and GPR40 were more strongly expressed in islets from RGZ-treated OLETF rats compared to control islets. Conclusion: These observations suggest that PPAR-γ activation with RGZ and/or adenoviral overexpression increased intracellular calcium mobilization, insulin secretion, and β-cell gene expression through GPR40 and GLUT2 gene up-regulation. 

Retracted: No

PubPeer comments:
 Figure 6. * Red boxes: a group of cells visible in the  RGZ+Plamitic acid panel in Figure 6A looks similar to a group of cells visible in the  Cont panel in Figure 6B. Reported to the journal in 2015. ![file] ,
Long noncoding RNA PTPRG-AS1 acts as a microRNA-194-3p sponge to regulate radiosensitivity and metastasis of nasopharyngeal carcinoma cells via PRC1
Authors: Xin-Ming Yang
Shuang Wang
Lei Ouyang
Shi-Sheng Li
Liang Yi
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: long noncoding RNA PTPRG-AS1; metastasis; microRNA-194-3p; nasopharyngeal carcinoma; protein regulator of cytokinesis 1
Affiliations: Department of Otolaryngology, Head and Neck Surgery, The Second Xiangya Hospital, Central South University, Changsha, People's Republic of China.

Abstract:  Protein regulator of cytokinesis 1 (PRC1) has been reported in correlation with various malignancies. Functionality of PRC1 in nasopharyngeal carcinoma (NPC) was investigated, in perspective of long noncoding RNA (lncRNA) regulatory circuitry. Aberrant expressed messenger RNA and lncRNA were screened out from the Gene Expression Omnibus microarray database. NPC cell line CNE-2 was adopted for in vitro study and transfected with mimic or short hairpin RNA of miR-194-3p and PTPRG-AS1. The radioactive sensitivity, cell viability, migration, invasion, and apoptosis were detected. PTPRG-AS1 and PRC1 were upregulated in NPC, whereas miR-194-3p was downregulated. PTPRG-AS1 was found to specifically bind to miR-194-3p as a competing endogenous RNA and miR-194-3p targets and negatively regulates PRC1. Overexpressed miR-194-3p or silenced PTPRG-AS1 resulted in enhanced sensitivity to radiotherapy and cell apoptosis along with suppressed cell migration, invasion and proliferation in NPC. Furthermore, impaired tumor formation was also caused by miR-194-3p overexpression or PTPRG-AS1 suppression through xenograft tumor in nude mice. In our study, PTPRG-AS1/miR-194-3p/PRC1 regulatory circuitry was revealed in NPC, the mechanism of which can be of clinical significance for treatment of NPC. 

Retracted: No

PubPeer comments:
 ![file] ,
An Artificially Designed Interfering lncRNA Expressed by Oncolytic Adenovirus Competitively Consumes OncomiRs to Exert Antitumor Efficacy in Hepatocellular Carcinoma
Authors: Mengchao Wu
Bin Sun
Zhangxiao Peng
Yinghan Su
Xiaoya Li
Weidan Ji
Yang Xu
Changqing Su
Journal: Molecular Cancer Therapeutics (2016)
Discipline: CLINICAL MEDICINE
Keywords: miRNAs; oncomiRs; lncRNAi; adenovirus; hepatocellular carcinoma
Affiliations: Department of Molecular Oncology, Eastern Hepatobiliary Surgical Hospital & National Center for Liver Cancer, Second Military Medical University, Shanghai, China., School of Life Science, University of Liverpool, Liverpool, United Kingdom., Department of Molecular Oncology, Eastern Hepatobiliary Surgical Hospital & National Center for Liver Cancer, Second Military Medical University, Shanghai, China. Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Xuzhou Medical College, Xuzhou, China. .

Abstract:  Endogenous miRNAs, especially oncogenic miRNAs (OncomiR), have been molecular targets for cancer therapy. We generated an artificially designed interfering long noncoding RNA (lncRNAi), which contains the sequences that can complementarily bind to multiple OncomiRs and is expressed by cancer-selectively replicating adenovirus. The adenovirus-expressed lncRNAi with high levels in hepatocellular carcinoma (HCC) cells competes with OncomiR target genes to bind to and consume OncomiRs, thereby achieving the targeted anti-HCC efficacy. With the targeting replication of adenovirus in HCC cells, lncRNAi was highly expressed and resulted in decreased abilities of proliferation, migration, and invasion, induced cell-cycle changes and apoptosis, and markedly changed the cellular mRNA and miRNA expression profiles in HCC cells. The optimal antitumor effect was also demonstrated on HCC cell line xenograft models and HCC patient-derived xenograft (PDX) tumor models in nude mice. This strategy has established a technology platform with a reliable therapeutic effect for HCC therapy. Mol Cancer Ther; 15(7); 1436-51. ©2016 AACR. 

Retracted: No

PubPeer comments:
 Concern about Figure 3B. It appears to show several areas of overlap, as highlighted here. Could the authors please comment? ![file] , 
 We sincerely apologize for our negligence, we also appreciate Pubpeer s action to point out our mistake and urging us to be more careful in our future work. We have already contacted the journal editorial board to correct the error. , 
 #2 Do the authors have an update? There appear to me 10 or so papers with shared authors and shared concerns. https: pubpeer.com search?q=authors%3A%22Changqing+Su%22 ,
Perception of shape from shading
Authors: V S Ramachandran
Journal: Nature (1988)
Discipline: Multidisciplinary
Keywords: human visual system; three-dimensional orientation; shape from shading; perception; computational mechanisms
Affiliations: University of California, San Diego, La Jolla 92093.

Abstract:  The human visual system can rapidly and accurately derive the three-dimensional orientation of surfaces by using variations in image intensity alone. This ability to perceive shape from shading is one of the most important yet poorly understood aspects of human vision. Here we present several findings which may help reveal computational mechanisms underlying this ability. First, we find that perception of shape from shading is a global operation which assumes that there is only one light source illuminating the entire visual image. This implies that if two identical objects are viewed simultaneously and illuminated from different angles, then we would be able to perceive three-dimensional shape accurately in only one of them at a time. Second, three-dimensional shapes that are defined exclusively by shading can provide tokens for the perception of apparent motion, suggesting that the motion mechanism is remarkably versatile in the kinds of inputs it can use. Lastly, the occluding edges which delineate an object from its background can also powerfully influence the perception of three-dimensional shape from shading. 

Retracted: No

PubPeer comments:
 I discuss this paper and the conceptual problems with treating  shading as a  cue to shape and depth in a new preprint https: psyarxiv.com rdksx . ,
EGCG inhibits mammary cancer cell migration through inhibition of nitric oxide synthase and guanylate cyclase
Authors: Thejass Punathil
Santosh K Katiyar
Trygve O Tollefsbol
Journal: Biochemical and biophysical research communications (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Tumor cell migration; (-)-epigallocatechin-3-gallate (EGCG); 4T1 cells; nitric oxide synthase; endogenous NO/NOS
Affiliations: Department of Dermatology, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall 557, Birmingham, AL, USA.

Abstract:  Tumor cell migration is considered as a major event in the metastatic cascade. Here we examined the effect of (-)-epigallocatechin-3-gallate (EGCG) on migration capacity and molecular mechanism using 4T1 murine mammary cancer cells as a model. Using an in vitro migration assay, we found that treatment of 4T1 cells with EGCG resulted in concentration-dependent inhibition of migration of these cells. The migration capacity of cells was reduced in presence of N(G)-nitro-l-arginine methyl ester (l-NAME), an inhibitor of nitric oxide synthase. EGCG suppressed the elevated levels of endogenous NO/NOS in 4T1 cells and blocked the migration promoting capacity of l-arginine. Treatment with guanylate cyclase inhibitor 1-H-[1,2,4]oxadiaxolo[4,3-a]quinolalin-1-one (ODQ) reduced the migration of 4T1 cells. EGCG reduced the elevated levels of cGMP in cancer cells and blocked the migration restoring activity of 8-Br cGMP (cGMP analogue). These results indicate for the first time that EGCG inhibits mammary cancer cell migration through the inhibition of NO/NOS and guanylate cyclase. 

Retracted: No

PubPeer comments:
 This study contains minor amount of contamination. Figure 4 shows the presence of Delftia, which is normally considered a contamination in human associated environments. Supplementary figure 4 also shows marine Shewanella, which seem unlikely to be present (together with Streptococcus marimammalium and Halomonas species). This seems to only affect the data from the small intestine, which has considerable less biomass than fecal content. The fecal data seems to be unaffected. ,
Lewy pathological study on α-synuclein in gastrointestinal tissues of prodromal Parkinson's disease
Authors: W-F Luo
H-P Zhang
Q-B Lu
Z-F Zhu
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Lewy pathological study; α-synuclein; gastrointestinal tissues; prodromal Parkinson's disease; withdrawn
Affiliations: Department of Neurology, the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China. .

Abstract:  The article "Lewy pathological study on α-synuclein in gastrointestinal tissues of prodromal Parkinson's disease" by Q.-B. Lu, Z.-F. Zhu, H.-P. Zhang, W.-F. Luo, published in Eur Rev Med Pharmacol Sci 2017; 21 (7): 1514-1521 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
EHMT2 promotes the development of prostate cancer by inhibiting PI3K/AKT/mTOR pathway
Authors: Y Lin
Y-Y Shi
X-P Yang
H-T Fan
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: EHMT2; prostate cancer; prognosis; qRT-PCR; PI3K/AKT/mTOR pathway
Affiliations: Department of Urological Surgery, the Second Affiliated Hospital of Jilin University, Changchun, China. .

Abstract:  Objective: To investigate the expression characteristics and the potential role of euchromatic histone-lysine N-methyltransferase 2 (EHMT2) in the clinical pathology and prognosis of prostate cancer (PCa). Patients and methods: Quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of EHMT2 in 55 pairs of PCa tissues and adjacent normal tissues. The relationship between EHMT2 expression and the pathological features, as well as the prognosis of PCa patients was analyzed. EHMT2 expression in PCa cells was determined by qRT-PCR as well. In addition, EHMT2 knockdown model was constructed by transfection of the small interfering RNA in PCa cell lines PC-3 and DU-145. The regulatory effects of EHMT2 on the behaviors of PCa cells were evaluated through cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU), colony formation assay and flow cytometry. Finally, we detected the protein levels of relative genes in PI3K/AKT/mTOR pathway through Western blot. Results: QRT-PCR results showed that the expression level of EHMT2 in PCa tissues was markedly higher than that in adjacent normal tissues. Compared with PCa patients with low expression of EHMT2, those with high expression of EHMT2 had higher pathological grade and lower overall survival. EHMT2 was also highly expressed in PCa cell lines. Knockdown of EHMT2 inhibited the proliferative potential and induced apoptosis of PCa cells. Western blot results revealed that PCa cells with EHMT2 knockdown presented downregulated p-PI3K, p-AKT and p-mTOR. Conclusions: EHMT2 was highly expressed in PCa, and its expression is closely correlated with tumor stage and poor prognosis of PCa patients. EHMT2 promoted the malignant progression of PCa by inhibiting PI3K/AKT/mTOR pathway. 

Retracted: No

PubPeer comments:
 Fig 1D.  Survival analysis of PCa patients based on their expressions of EHMT2 . ![file] Another manifestation of  Hoya s Law for J.BUOn ERMPS :  When 40 or 50 cases of any given cancer are dichotomised into half-groups of high- or low-expression of any given noncoding RNA, survival rate for one half-group or both *always* drops to 0% at 75 months. Some other examples, from left to right: - Fig 1 from [Zang et al (2020)] - Fig 1 from [Li et al (2020)] - Fig 1, and Fig 4D, from [Cui et al (2019)] - Fig 1D from [Gao et al (2019)] . ![file] *[left]* Figure 1C from [Wu et al (2020)] . *[right]* Figs 1D, 3E from [Wu et al (2019)] . ![file] 1D from [Luo, Yan Liu] : ![] ,
Evaluation of structure, chaperone-like activity and protective ability of peroxynitrite modified human α-Crystallin subunits against copper-mediated ascorbic acid oxidation
Authors: Kazem Khoshaman
Maryam Ghahramani
Boris I Kurganov
Reza Yousefi
Sogand Sasan Moghadam
Journal: International Journal of Biological Macromolecules (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Ascorbic acid; Chaperone activity; Copper ion; Peroxynitrite; α-Crystallin.

Abstract:  The copper-catalyzed oxidation of ascorbic acid (ASA) to dehydroascorbate (DHA) and hydrogen peroxide plays a central role in pathology of cataract diseases during ageing and in diabetic patients. In the current study, the structural feature, chaperone-like activity and protective ability of peroxynitrite (PON) modified αA- and αB-Crystallin (Cry) against copper-mediated ASA oxidation were studied using different spectroscopic measurements and gel mobility shift assay. Upon PON modification, additional to protein structural alteration, the contents of nitrotyrosine, nitrotryptophan, dityrosine and carbonyl groups were significantly increased. Moreover, αB-Cry demonstrates significantly larger capacity for PON modification than αA-Cry. Also, based on the extent of PON modification, these proteins may display an improved chaperone-like activity and enhanced protective ability against copper-mediated ASA oxidation. In the presence of copper ions, chaperone-like activity of both native and PON-modified α-Cry subunits were appreciably improved. Additionally, binding of copper ions to native and PON-modified proteins results in the significant reduction of their solvent exposed hydrophobic patches. Overall, the increase in chaperone-like activity/ASA protective ability of PON-modified α-Cry and additional enhancement of its chaperoning action with copper ions appear to be an important defense mechanism offered by this protein. 

Retracted: No

PubPeer comments:
 In Figure 5 and 6, several graphs are reused. In Figure 7, the size distribution is duplicated but the numbers are different. ![file] ![file] ,
GIV is a nonreceptor GEF for G alpha i with a unique motif that regulates Akt signaling
Authors: Marilyn G Farquhar
Mikel Garcia-Marcos
Pradipta Ghosh
Journal: Proceedings of the National Academy of Sciences of the United States of America (2009)
Discipline: Multidisciplinary
Keywords: Heterotrimeric G proteins; signal transduction; G protein-coupled receptors; guanine nucleotide exchange factors (GEFs); GIV/Girdin
Affiliations: Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA.

Abstract:  Heterotrimeric G proteins are molecular switches that control signal transduction. Ligand-occupied, G protein-coupled receptors serve as the canonical guanine nucleotide exchange factors (GEFs) that activate heterotrimeric G proteins. A few unrelated nonreceptor GEFs have also been described, but little or nothing is known about their structure, mechanism of action, or cellular functions in mammals. We have discovered that GIV/Girdin serves as a nonreceptor GEF for G alpha i through an evolutionarily conserved motif that shares sequence homology with the synthetic GEF peptide KB-752. Using the available structure of the KB-752 x G alpha i1 complex as a template, we modeled the G alpha i-GIV interface and identified the key residues that are required to form it. Mutation of these key residues disrupts the interaction and impairs Akt enhancement, actin remodeling, and cell migration in cancer cells. Mechanistically, we demonstrate that the GEF motif is capable of activating as well as sequestering the G alpha-subunit, thereby enhancing Akt signaling via the G betagamma-PI3K pathway. Recently, GIV has been implicated in cancer metastasis by virtue of its ability to enhance Akt activity and remodel the actin cytoskeleton during cancer invasion. Thus, the novel regulatory motif described here provides the structural and biochemical basis for the prometastatic features of GIV, making the functional disruption of this unique G alpha i-GIV interface a promising target for therapy against cancer metastasis. 

Retracted: No

PubPeer comments:
 Blots from different treatments appear to be different exposures of the same samples.![](http: ) ![file] , 
 Hi, I am the first author of this manuscript and I just came across this post by chance. Thanks for identifying this oversight on our side. I was able to locate the original files from 12 years ago, and below you can find an amended figure that has the correct Actin blot in panel B. Best regards, Mikel ![file] ,
Pro-caspase-3 overexpression sensitises ovarian cancer cells to proteasome inhibitors
Authors: M Marani
I McNeish
T Tenev
N R Lemoine
Journal: Cell death and differentiation (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ubiquitin-proteasome pathway; apoptosis; proteasome inhibitors; caspase-3; ovarian cancer
Affiliations: ICRF Molecular Oncology Unit, Imperial College School of Medicine at Hammersmith Hospital, London W12 ONN, UK.

Abstract:  The ubiquitin-proteasome pathway plays a critical role in the degradation of several proteins involved in the cell cycle. Dysregulation of this pathway leads to inhibition of cellular proliferation and the induction of apoptosis. Ubiquitination and its downstream consequences have been investigated intensively as targets for the development of drugs for tumour therapy. Here we have investigated the mechanism of apoptosis induced by the proteasome inhibitors MG-132, lactacystin and calpain inhibitor I (ALLN), in the HEK 293 cell line and the ovarian cancer cell lines SKOV3 and OVCAR3. We have found strong caspase-3-like and caspase-6-like activation upon treatment of HEK 293 cells with MG-132. Using a tricistronic expression vector based on a tetracycline-responsive system we generated stable SKOV3 nd OVCAR3 cell lines with inducible expression of pro-caspase-3. Induction of pro-caspase-3 expression in normally growing cells does not induce apoptosis. However, in the presence of the proteasome inhibitors MG-132, lactacystin or ALLN we found that cells overexpressing pro-caspase-3 are rapidly targeted for apoptosis. Our results demonstrate that pro-caspase-3 can sensitise ovarian cancer cells to proteasome inhibitor-induced apoptosis, and a combination of these approaches might be exploited for therapy of ovarian and other cancers. 

Retracted: No

PubPeer comments:
 This paper claims to test TRAF6 levels in Human Cardiomyocytes (HCM), with primer sequences: **TRAF6: forward 5u2019-CAG TGG TCG TAT CGT GCT TA3u2032, reverse 5u2019-CCT TAT GGT TTC TTG GAG TC-3u2032** In Fig.1E, it shows mRNA levels of Traf6 in a rat model of disease: ![file] **Analysis of this primer pair for rat groups, shows these:** ![file] **Analysis of the primer pair for HCMs shows these:** ![file] **Google scholar search shows that these 2 primers are found in a mollusc, for the same Traf6 gene.** ![file] The organism the Goougle scholar results refer to: ![file] *Image Source: http: mgb.ouc.edu.cn cfbase html * Could the authors please explain if there was a lack of sharing the Traf6 primers for human cells and rat ones and how is it possible that this primer pair was used in 2 other studies for a completely different non-mammal organism? ,
Antitumor Activity of 2,9-Di-Sec-Butyl-1,10-Phenanthroline
Authors: Jack F Eichler
Shifang Peng
Nabil F Saba
Sreenivas Nannapaneni
Mohammad Aminur Rahman
Yuan Liu
Zhuo G Chen
Dong M Shin
Dongsheng Wang
A R M Ruhul Amin
Journal: PLoS ONE (2016)
Discipline: Multidisciplinary
Keywords: chelating phen-based ligand; dsBPT; lung cancer; head and neck cancer; cell cycle
Affiliations: Department of Hematology and Medicinal Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, United States of America., Department of Biostatistics and Bioinformatics, Biostatistics and Bioinformatics Shared Resource at WCI, NE, Atlanta, GA, United States of America., Department of Chemistry, University of California-Riverside, Riverside, CA, United States of America.

Abstract:  The anti-tumor effect of a chelating phen-based ligand 2,9-di-sec-butyl-1,10-phenanthroline (dsBPT) and its combination with cisplatin were examined in both lung and head and neck cancer cell lines and xenograft animal models in this study. The effects of this agent on cell cycle and apoptosis were investigated. Protein markers relevant to these mechanisms were also assessed. We found that the inhibitory effect of dsBPT on lung and head and neck cancer cell growth (IC50 ranged between 0.1-0.2 μM) was 10 times greater than that on normal epithelial cells. dsBPT alone induced autophagy, G1 cell cycle arrest, and apoptosis. Our in vivo studies indicated that dsBPT inhibited tumor growth in a dose-dependent manner in a head and neck cancer xenograft mouse model. The combination of dsBPT with cisplatin synergistically inhibited cancer cell growth with a combination index of 0.3. Moreover, the combination significantly reduced tumor volume as compared with the untreated control (p = 0.0017) in a head and neck cancer xenograft model. No organ related toxicities were observed in treated animals. Our data suggest that dsBPT is a novel and potent antitumor drug that warrants further preclinical and clinical development either as a single agent or in combination with known chemotherapy drugs such as cisplatin. 

Retracted: No

PubPeer comments:
 Figure 6 appears to have a repeated image. *** ![file] *** Closeup ![file] , 
 Erratum We thank PUBPEER for finding the duplicate image in our publication. We found the control (CNT) image was misplaced. Though it does not affect the overall results, we sincerely apologize for this careless mistake and any inconvenience caused to the journal. We have notified the journal and provided the corrected figure. Since the figure size is more than 1M, we cannot attach it here. Please let us know if any further action is required. Sincerely, Zhuo G. Chen, Ph.D. Corresponding Author , 
 #2 Dr. Chen: Thank you for your reply and intention to correct the figure. No further action is necessary. Best wishes. ,
Endothelial-Rac1 is not required for tumor angiogenesis unless alphavbeta3-integrin is absent
Authors: Stephen D Robinson
Gabriela D&#x27;Amico
Georgia Mavria
Mitchel Germain
Marcus Fruttiger
Gareth J Thomas
Garry Saunders
Victor Tybulewicz
Louise E Reynolds
Kairbaan M Hodivala-Dilke
George Elia
Journal: PLoS ONE (2010)
Discipline: Multidisciplinary
Keywords: Endothelial cell migration; Rac1 activity; tumor angiogenesis; VEGF-mediated angiogenesis; chemotactic migratory responses
Affiliations: Adhesion and Angiogenesis Laboratory, Institute of Cancer, Bart's and The London, Queen Mary's School of Medicine and Dentistry, London, United Kingdom. 

Abstract:  Endothelial cell migration is an essential aspect of tumor angiogenesis. Rac1 activity is needed for cell migration in vitro implying a requirement for this molecule in angiogenesis in vivo. However, a precise role for Rac1 in tumor angiogenesis has never been addressed. Here we show that depletion of endothelial Rac1 expression in adult mice, unexpectedly, has no effect on tumor growth or tumor angiogenesis. In addition, repression of Rac1 expression does not inhibit VEGF-mediated angiogenesis in vivo or ex vivo, nor does it affect chemotactic migratory responses to VEGF in 3-dimensions. In contrast, the requirement for Rac1 in tumor growth and angiogenesis becomes important when endothelial beta3-integrin levels are reduced or absent: the enhanced tumor growth, tumor angiogenesis and VEGF-mediated responses in beta3-null mice are all Rac1-dependent. These data indicate that in the presence of alphavbeta3-integrin Rac1 is not required for tumor angiogenesis. 

Retracted: No

PubPeer comments:
 Fig 2. ![file] The bizarrely stylised flow-cytometry plots, and the equally stylised Western Blots, locate this paper within the output of the  tadpole papermill . ,
Role and mechanism of microRNA-548c-3p/c-Myb in myocardial infarction fibrosis in rats
Authors: J Wang
S-H Zhang
C-Q Wang
L-X Zhang
Z Zhao
L Zhang
Q Bing
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-548c-3p; myocardial fibrosis; c-Myb; myocardial infarction; in-vivo
Affiliations: Department of Gerontology, The Third Hospital of Hebei Medical University, Shijiazhuang, China. .

Abstract:  Objective: To investigate the role of micro ribonucleic acid (miR)-548c-3p in myocardial fibrosis after myocardial infarction (MI), and to explore the possible underlying. Materials and methods: The rat model of MI was successfully established in-vivo. MiR-548c-3p was upregulated via lentivirus transfection with miR-548c-3p mimics. Cardiac function of rats was detected via echocardiography. Meanwhile, Sirius red and Masson staining were used to detect the level of fibrosis index in MI model. Subsequently, myocardial fibroblasts were isolated and cultured in vitro. An oxygen-glucose deprivation (OGD) model was established to mimicking the ischemic condition. Furthermore, the relationship between miR-548c-3p and c-Myb was verified, and the levels of fibrosis-related factors (including α-SMA and COL1A1) were measured. Results: In-vivo experiments showed that miR-548c-3p expression in rats was significantly down-regulated at 2 and 4 weeks after MI. Up-regulation of miR-548c-3p significantly improved cardiac function, reduced myocardial fibrosis and inhibited the protein expression of proto-oncogene c-Myb (c-Myb). In vitro experiments revealed that c-Myb was a target gene of miR-548c-3p. In addition, miR-548c-3p could inhibit the expressions of α-SMA and COL1A1 through targeting c-Myb. Conclusions: MiR-548c-3p could improve myocardial fibrosis by targeting c-Myb. 

Retracted: No

PubPeer comments:
 Below: Figure 2A.  Up-regulation of miR-548c-3p improved cardiac function after infarction. A, Representative transthoracic M-mode echocardiograms from each group. . Above: Figure 2A from [Wu et al (2019)] .  Sitagliptin improves the myocardial function of rats. A, M-mode echocardiogram of rats in each group . I have concerns. ![file] ,
STAT3 inhibitor WP1066 attenuates miRNA-21 to suppress human oral squamous cell carcinoma growth in vitro and in vivo
Authors: Lei Han
Shasha Li
Aiqin Liu
Yu Ren
Ping Li
Xudong Wang
Lun Zhang
Xuan Zhou
Kailiang Zhang
Chunsheng Kang
Peng Li
Journal: Oncology Reports (2014)
Discipline: CLINICAL MEDICINE
Keywords: STAT3; miR-21; OSCC; WP1066; tumor cell proliferation
Affiliations: Department of Otorhinolaryngology and Maxillofacial Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, P.R. China., Tianjin Research Center of Basic Medical Science, Tianjin Medical University, Tianjin 300070, P.R. China., Department of Otorhinolaryngology and Maxillofacial Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China., Tianjin Medical University General Hospital, Laboratory of Neuro-Oncology, Tianjin Neurological Institute, Tianjin 300052, P.R. China., Tianjin Medical Information Institute, Tianjin 300070, P.R. China., Key Laboratory of Cancer Prevention and Therapy, Tianjin Cancer Institute, Tianjin 300060, P.R. China.

Abstract:  Abnormalities in signal transducer and activator of transcription 3 (STAT3) are involved in the oncogenesis of oral squamous cell carcinoma (OSCC). MicroRNA-21 (miR-21) is an important gene expression regulator to OSCC. miR-21 induction by STAT3 has been reported in multiple human cancers. In the present study, we found that STAT3 (-/p) expression was positively correlated with miR-21 in 60 OSCC samples. A reporter gene assay showed that miR-21 overexpression was dependent on STAT3 activation. WP1066, a small molecular inhibitor of STAT3, was used to suppress STAT3 expression in OSCC cells. TSCCA and TCA8113 showed reduction in tumor cell proliferation, invasion ability and miR-21 expression by WP1066 treatment. In addition, the expression of miR-21 target proteins [programmed cell death 4 (PDCD4), tissue inhibitor of metalloproteinase 3 (TIMP-3) and phosphatase and tensin homolog (PTEN)] was upregulated. Restored STAT3 expression by IL-6 induced miR-21 overexpression, which further confirmed the correlation between STAT3 and miR-21. WP1066 inhibited tumor growth and induced tumor cell apoptosis in the TSCCA xenograft tumor model. Western blotting and immunohistochemistry staining indicated that STAT3 (-/p), Ki67, Bcl-2 and MMP-2 expressions decreased in the WP1066-treated group; PDCD4, TIMP-3 and PTEN expression increased simulta-neously. The present study provides evidence that targeting STAT3 could regulate OSCC cell growth in a miR-21-dependent manner and WP1066 could be a novel candidate drug to treat OSCC by inhibiting STAT3/miR-21 axis. 

Retracted: No

PubPeer comments:
 The XRD pattern of the alloyed composition Cu + TiO2 appears to be exactly the same as that of a Cu + Cr2O3 alloy. Even the noise in the two XRD patterns is the same! ![file] Compare the following; Figure 3 in: https: doi.org 10.1016 j.jallcom.2016.12.180 Figure 4 in: https: doi.org 10.1016 j.powtec.2012.02.001 ,
Sensor kinase KinB and its pathway-associated key factors sense the signal of nutrition starvation in sporulation of Bacillus subtilis
Authors: Xiaowei Huang
Feng Gao
Jinyuan Yan
Weipeng Liu
Zeying He
Journal: MicrobiologyOpen (2018)
Discipline: MICROBIOLOGY
Keywords: KapB; KbaA; environmental signal; nutrient starvation; sensor kinase KinB
Affiliations: State Key Laboratory for Conservation and Utilization of Bio-Resources, and Key Laboratory for Microbial Resources of the Ministry of Education, Yunnan University, Kunming, Yunnan, China., Yunnan Institute of Tropical Crops, Jinghong, Yunnan, China., Center Laboratory of the Second Hospital affiliated with Kunming Medical University, Kunming, China.

Abstract:  Bacillus subtilis responds to environmental stress cues and develops endospores for survival. In the process of endospore formation, sporulation initiation is a vital stage and this stage is governed by autophosphorylation of the sensor histidine kinases. The second major sensor kinase KinB perceives the intracellular changes of GTP and ATP during sporulation. However, determination of the environmental signals as well as its related signaling pathway of KinB requires further elucidation. Our current study found that, contrary to the sporulation failure induced by ΔkinA in the nutrient-rich 2× SG medium, the sensor kinase KinB sensed the environmental cues in the nutrient-poor MM medium. Two other membrane proteins, KapB and KbaA, also responded similarly to the same external signal as KinB. Both KapB and KbaA acted upstream of KinB, but they exerted their regulation upon KinB independently. Furthermore, we demonstrated that both the SH3 domain and the α-helix structure in KapB are required for sensing or transducing the signal of sporulation initiation. Collectively, our work here supplied the direct evidences that KinB and its pathway sense the external signal of nutrient starvation in MM medium, and further analyzes the interrelationship among KinB, KbaA, and KapB. 

Retracted: No

PubPeer comments:
 Figure 5B. * Red arrows: Each of the bands appears surrounded by a rectangle with a sharp background transition, suggesting that the bands might not have been run adjacent to each other in the same gel. This makes it hard to compare band sizes and exposure times. Could the authors please submit the raw, unprocessed blot image here? Posting that here might take away any concerns - sometimes those lines could be caused e.g. by image processing. ![file] Brought to my attention via Twitter. https: twitter.com christo71213435 status 1375929988285882368 ,
A comparative review of cell culture systems for the study of microglial biology in Alzheimer's disease
Authors: Jan Post
Kenneth Hensley
Branden Stansley
Journal: Journal of neuroinflammation (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer's disease; microglia; cell culture techniques; primary microglia; immortalized cell lines
Affiliations: Department of Neurosciences, University of Toledo Medical Center, Toledo, OH, USA.

Abstract:  Over the past two decades, it has become increasingly apparent that Alzheimer's disease neuropathology is characterized by activated microglia (brain resident macrophages) as well as the classic features of amyloid plaques and neurofibrillary tangles. The intricacy of microglial biology has also become apparent, leading to a heightened research interest in this particular cell type. Over the years a number of different microglial cell culturing techniques have been developed to study either primary mammalian microglia, or immortalized cell lines. Each microglial system has advantages and disadvantages and should be selected for its appropriateness in a particular research context. This review summarizes several of the most common microglial cell culture systems currently being employed in Alzheimer's research including primary microglia; BV2 and N9 retroviral immortalized microglia; human immortalized microglia (HMO6); and spontaneously immortalized rodent microglial lines (EOC lines and HAPI cells). Particularities of cell culture requirements and characteristics of microglial behavior, especially in response to applied inflammogen stimuli, are compared and discussed across these cell types. 

Retracted: No

PubPeer comments:
null, 
 TIL  murine means mice but also rats or other related rodents. https: www.merriam-webster.com dictionary murine ,
RETRACTED ARTICLE: Age-dependent Increase in Desmosterol Restores DRM Formation and Membrane-related Functions in Cholesterol-free DHCR24−/− Mice
Authors: Fabienne Skaanes-Brunner
Dieter Lütjohann
Karin M Thelen
Katrin Kuehnle
M Hasan Mohajeri
Lucie Kalvodova
Luka Kulic
Arames Crameri
Maria D Ledesma
Alicia E Smith
Frank L Heppner
Roger M Nitsch
Journal: Neurochemical Research (2009)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Cholesterol; DHCR24; Membrane composition; Desmosterol; DRM structure
Affiliations: Division of Psychiatry Research, University of Zurich, Zurich, Switzerland. 

Abstract:  Cholesterol is a prominent modulator of the integrity and functional activity of physiological membranes and the most abundant sterol in the mammalian brain. DHCR24-knock-out mice lack cholesterol and accumulate desmosterol with age. Here we demonstrate that brain cholesterol deficiency in 3-week-old DHCR24(-/-) mice was associated with altered membrane composition including disrupted detergent-resistant membrane domain (DRM) structure. Furthermore, membrane-related functions differed extensively in the brains of these mice, resulting in lower plasmin activity, decreased beta-secretase activity and diminished Abeta generation. Age-dependent accumulation and integration of desmosterol in brain membranes of 16-week-old DHCR24(-/-) mice led to the formation of desmosterol-containing DRMs and rescued the observed membrane-related functional deficits. Our data provide evidence that an alternate sterol, desmosterol, can facilitate processes that are normally cholesterol-dependent including formation of DRMs from mouse brain extracts, membrane receptor ligand binding and activation, and regulation of membrane protein proteolytic activity. These data indicate that desmosterol can replace cholesterol in membrane-related functions in the DHCR24(-/-) mouse. 

Retracted: Yes

PubPeer comments:
 Erratum to: Neurochem Res (2009) 34:1167u20131182 DOI 10.1007 s11064-008-9893-4 Dear Dr. Lajtha: We received your email concerning republishing data in the Kuehnle et al., paper published in Neurochemical Research (34, 1167-1182). After careful review of the raw data, we indeed found that some Western blots shown had been used in a prior publication (Crameri et al., EMBO J., 25, 432-443). We cannot explain this error and very much regret this oversight. As a result, we propose to retract the publication in Neurochemical Research. I informed the coworkers and they all agreed with this decision. We sincerely apologize for our mistake and any inconvenience this might cause for the journal. Sincerely, Katrin Kuehnle Corresponding Author ,
Defective cellular trafficking of the bone morphogenetic protein receptor type II by mutations underlying familial pulmonary arterial hypertension
Authors: Lihadh Al-Gazali
Anne John
Praseetha Kizhakkedath
Bassam R Ali
Journal: Gene (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: BMPR2; ERAD; FPAH; Missense mutations; Protein misfolding.
Affiliations: Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates., Department of Pediatrics, College of Medicine and Heath Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates., Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates. Electronic address: .

Abstract:  Familial pulmonary arterial hypertension (FPAH) is a relatively rare but fatal disorder characterized by elevated arterial pressure caused by abnormal proliferation of endothelial cells of the arteries, which eventually leads to heart failure and death. FPAH is inherited as an autosomal dominant trait and is caused by heterozygous mutations in the BMPR2 gene encoding the bone morphogenetic protein type II receptor (BMPR2). BMPR2 belongs to the TGF β/BMP super-family of receptors involved in a signal transduction cascade via the SMAD signaling pathway. The BMPR2 polypeptide is composed of 1038 amino acids and consists of a ligand binding domain, a kinase domain and a cytoplasmic tail. To investigate the cellular and functional consequence of BMPR2 mutations, C-terminally FLAG-tagged constructs of eighteen pathogenic BMPR2 missense mutants were generated by site directed mutagenesis and expressed in HeLa and HEK-293T cell lines. The subcellular localizations of the mutant proteins were investigated using immunostaining and confocal microscopy. Post-translational modifications of the proteins were analyzed by Endoglycosidase H deglycosylation assay. Our results indicated that mutations in the ligand binding domain affecting highly conserved cysteine residues resulted in retention of the mutant proteins in the endoplasmic reticulum (ER), as evident from their co-localization with the ER resident protein calnexin. The kinase domain mutants showed both ER and plasma membrane (PM) distributions, while the cytoplasmic tail domain variants were localized exclusively to the PM. The subcellular localizations of the mutants were further confirmed by their characteristic glycosylation profiles. In conclusion, our results indicate that ER quality control (ERQC) is involved in the pathological mechanism of several BMPR2 receptor missense mutations causing FPAH, which can be explored as a potential therapeutic target in the future. 

Retracted: No

PubPeer comments:
 In Figure 5C, two of the immunoblots appear unexpectedly similar (marked by red boxes): ![file] For closer comparison, I enlarged the images and added another image of the left clone K512T with altered brightness and contrast: ![file] Could the authors please check their original data and if possible, provide the uncropped images of the blots? ,
Sympathetic activation causes focal adhesion signaling alteration in early compensated volume overload attributable to isolated mitral regurgitation in the dog
Authors: Mikhail A Kolpakov
Rachid Seqqat
Khadija Rafiq
Abdelkarim Sabri
Ray Dillon
Louis J Dell&#x27;italia
Journal: Circulation Research (2008)
Discipline: CLINICAL MEDICINE
Keywords: left ventricular; dilatation; mitral regurgitation; extracellular matrix; adrenergic drive
Affiliations: Cardiovascular Research Center, Temple University, MRB 801, 3420 N Broad St, Philadelphia, PA 19140, USA. , From the Cardiovascular Research Center (A.S., K.R., R.S., M.A.K.), Department of Anatomy &amp; Cell Biology, Temple University, Philadelphia, Pa; Auburn University of Veterinary Medicine (R.D.), Ala; and Departments of Medicine and Physiology and Biophysics (L.J.D.), University of Alabama, Birmingham.

Abstract:  We reported that left ventricular (LV) dilatation after 4 weeks of isolated mitral regurgitation (MR) in the dogs is marked by extracellular matrix loss and an increase in adrenergic drive. Given that extracellular matrix proteins and their receptor integrins influence beta-adrenergic receptor (beta-AR) responses in vitro, we tested whether beta1-AR activation modulates focal adhesion (FA) signaling and LV remodeling in these same dogs with isolated MR. Normal dogs were compared with dogs with MR of a 4-week duration and with MR dogs treated with beta(1)-AR blockade (beta(1)-RB) (extended-release metoprolol succinate, 100 mg QD) that was started 24 hours after MR induction. In MR LVs, a decrease in collagen accumulation compared with normal dogs was associated with a decrease in FA kinase tyrosine phosphorylation, along with FA kinase interaction with adapter and cytoskeletal proteins, p130(Cas) and paxillin, respectively, as determined by immunoprecipitation assays. There was increased phosphorylation of stress related molecules p38 mitogen-activated protein kinase (MAPK) and Hsp27 and survival signaling kinases extracellular signal-regulated kinase 1/2 and AKT, with no evidence of cardiomyocyte apoptosis. beta(1)-RB attenuated FA signaling loss and prevented p38 MAPK, Hsp27, and AKT phosphorylation induced by MR and significantly increased LV epicardial collagen content. However, beta(1)-RB did not improve LV endocardial collagen loss or LV dilatation induced by MR. Isolated myocytes from normal and MR dog hearts treated with beta(1)- or beta(2)-AR agonists demonstrated no difference in FA kinase, p38 MAPK, Hsp27, or AKT phosphorylation. These results showed that chronic stimulation of beta(1)-AR during early compensated MR impairs FA signaling that may affect myocyte/fibroblast-extracellular matrix scaffolding necessary for LV remodeling. 

Retracted: No

PubPeer comments:
 Figures 3 and 4 appear to be identical, although their legends are different. Could the authors please check if Figure 4 uploaded correctly? ![file] ,