PReD-Bench/PRed-Bench huggingface dataset:
A polysaccharide from Grifola frondosa fruit body induces HT-29 cells apoptosis by PI3K/AKT-MAPKs and NF-Œ∫B-pathway
Authors: Xu Wang
Nana Bie
Chunling Wang
Yanting Wang
Lirong Han
Journal: International Journal of Biological Macromolecules (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Grifola frondosa polysaccharide; HT-29 cells; Tumor suppressive activity.
Affiliations: State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Food Nutrition and Safety, Ministry of Education, College of Food Engineering and Biotechnology, Tianjin University of Science and Technology, No.29, 13th Avenue, Tianjin Economy Technological Development Area, Tianjin 300457, People's Republic of China., State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Food Nutrition and Safety, Ministry of Education, College of Food Engineering and Biotechnology, Tianjin University of Science and Technology, No.29, 13th Avenue, Tianjin Economy Technological Development Area, Tianjin 300457, People's Republic of China. Electronic address: .

Abstract:  Background: A neutral polysaccharide was isolated from the fruiting body of a mushroom Grifola frondosa (GFP-A). The tumor suppressive activity of GFP-A on protein expressions of PI3K/AKT, MAPKs, nuclear factor Œ∫B and caspase pathways in HT-29 cells were investigated. Methods: The inhibitory effect and mechanism of GFP-A on the HT-29 cells were investigated. The cell viability was examined by MTT. Scanning electron microscopy analysis and flow cytometry were conducted to examine the apoptosis of cells. The protein expressions of PI3K/AKT, MAPKs, nuclear factor Œ∫B and caspase pathways were analyzed using western blot. Results: The results of MTT assay showed that GFP-A of 180 Œºg/mL could significantly inhibit the proliferation of HT-29 cells. Western blotting results showed that GFP-A decreased the protein expression of PI3K and AKT, enhanced the phosphorylation of c-Jun N-terminal kinase (JNK), p38 MAPK and inhibited the phosphorylation of ERK1/2 and the translocation of nuclear factor-Œ∫B (NF-Œ∫B) into the nucleus. In the meanwhile, GFP-A could up-regulate the ratio of Bax to Bcl-2, increase the release of cytochrome C to cytoplasm, ultimately lead to the activation of caspase-9. Conclusions: The above results confirmed that GFP-A promoted the apoptosis of HT-29 cells through PI3K/AKT-MAPKs-NF-Œ∫B and caspase signaling pathways. 

Retracted: No

PubPeer comments:
 This paper is computer-generated. It is a very cool mix of [Scigen] [Mathgen] . The reference section is not randomly generated... Suggesting citation manipulation.  --- This comment was written by Guillaume Cabanac and Cyril Labbu00e9. Contact: [SeekAndBlastn-Operators@univ-grenoble-alpes.fr](mailto:SeekAndBlastn-Operators@univ-grenoble-alpes.fr). ,
Histone Deacetylase Inhibitors Impair Vasculogenic Mimicry from Glioblastoma Cells
Authors: Adriana Bajetto
Tullio Florio
Alessandro Mancini
Maria Teresa Gentile
Olga Pastorino
Luca Colucci-D&#x27;Amato
Antonella Di Costanzo
Paola Franco
Lucia Altucci
Maria Patrizia Stoppelli
Nunzio Del Gaudio
Journal: Cancers (2019)
Discipline: CLINICAL MEDICINE
Keywords: HDAC; angiogenesis; cancer stem cells; cell invasion; cell migration
Affiliations: Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania "Luigi Vanvitelli", 81100 Caserta, Italy. ., Department of Translational Medical Sciences, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. ., BioUp Sagl, 6900 Lugano, Switzerland. ., Department of Precision Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy. ., Pharmacology Unit, Department of Internal Medicine and Centre of Excellence for Biomedical Research (CEBR), University of Genova, 16132 Genova, Italy. ., IRCCS Ospedale Policlinico San Martino, 16132 Genova, Italy. ., Institute of Genetics and Biophysics "A. Buzzati Traverso" (IGB-ABT), National Research Council of Italy, 80131 Naples, Italy. ., InterUniversity Center for Research in Neurosciences (CIRN), 80131 Naples, Italy. .

Abstract:  Glioblastoma (GBM), a high-grade glioma (WHO grade IV), is the most aggressive form of brain cancer. Available treatment options for GBM involve a combination of surgery, radiation and chemotherapy but result in a poor survival outcome. GBM is a high-vascularized tumor and antiangiogenic drugs are widely used in GBM therapy as adjuvants to control abnormal vasculature. Vasculogenic mimicry occurs in GBM as an alternative vascularization mechanism, providing a means whereby GBM can escape anti-angiogenic therapies. Here, using an in vitro tube formation assay on Matrigel¬Æ, we evaluated the ability of different histone deacetylase inhibitors (HDACis) to interfere with vasculogenic mimicry. We found that vorinostat (SAHA) and MC1568 inhibit tube formation by rat glioma C6 cells. Moreover, at sublethal doses for GBM cells, SAHA, trichostatin A (TSA), entinostat (MS275), and MC1568 significantly decrease tube formation by U87MG and by patient-derived human GBM cancer stem cells (CSCs). The reduced migration and invasion of HDACis-treated U87 cells, at least in part, may account for the inhibition of tube formation. In conclusion, our results indicate that HDACis are promising candidates for blocking vascular mimicry in GBM. 

Retracted: No

PubPeer comments:
 There appears to be an image used for 2 different purposes - in Figure 1A (L) and Figure 2A (R). TAM. ***  ,
Inhibition of tumor vasculogenic mimicry and prolongation of host survival in highly aggressive gallbladder cancers by norcantharidin via blocking the ephrin type a receptor 2/focal adhesion kinase/paxillin signaling pathway
Authors: Jing-Tao Zhang
Wei Sun
Yue-Zu Fan
Wen-Zhong Zhang
Hui Wang
Chun-Yan Ge
Zhong-Yan Liu
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Vasculogenic mimicry; Gallbladder cancers; Norcantharidin; EphA2; FAK
Affiliations: Department of Surgery, Tongji Hospital, Tongji University School of Medicine, Tongji University, Shanghai, P.R. China., Department of Surgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Tongji University, Shanghai, P.R. China., Department of Surgery, Shanghai Pudong New Area People's Hospital, Shanghai, P.R. China., Department of Oncology, Shanghai Yangpu Geriatric Hospital, Shanghai, P.R. China.

Abstract:  Vasculogenic mimicry (VM) is a newly-defined tumor microcirculation pattern in highly aggressive malignant tumors. We recently reported tumor growth and VM formation of gallbladder cancers through the contribution of the ephrin type a receptor 2 (EphA2)/focal adhesion kinase (FAK)/Paxillin signaling pathways. In this study, we further investigated the anti-VM activity of norcantharidin (NCTD) as a VM inhibitor for gallbladder cancers and the underlying mechanisms. In vivo and in vitro experiments to determine the effects of NCTD on tumor growth, host survival, VM formation of GBC-SD nude mouse xenografts, and vasculogenic-like networks, malignant phenotypes i.e., proliferation, apoptosis, invasion and migration of GBC-SD cells. Expression of VM signaling-related markers EphA2, FAK and Paxillin in vivo and in vitro were examined by immunofluorescence, western blotting and real-time polymerase chain reaction (RT-PCR), respectively. The results showed that after treatment with NCTD, GBC-SD cells were unable to form VM structures when injecting into nude mouse, growth of the xenograft was inhibited and these observations were confirmed by facts that VM formation by three-dimensional (3-D) matrix, proliferation, apoptosis, invasion, migration of GBC-SD cells were affected; and survival time of the xenograft mice was prolonged. Furthermore, expression of EphA2, FAK and Paxillin proteins/mRNAs of the xenografts was downregulated. Thus, we concluded that NCTD has potential anti-VM activity against human gallbladder cancers; one of the underlying mechanisms may be via blocking the EphA2/FAK/Paxillin signaling pathway. 

Retracted: No

PubPeer comments:
 Figure 2. * Green boxes: Two panels appear to show an overlap * Yellow boxes: Two panels appear to show an overlap with a rotation Figure 7B * Red boxes: Two b-actin lanes appear to be visible twice in the same panel Figure 7A * Red arrows: Two square patches appear to be visible in the Control EphA2 panel Reported to the journal in October 2015, but no action as of today.  ,
Paeoniflorin-6‚Ä?O-benzene sulfonate down-regulates CXCR4-GŒ≤Œ≥-PI3K/AKT mediated migration in fibroblast-like synoviocytes of rheumatoid arthritis by inhibiting GRK2 translocation
Authors: Wu Wang
Meng-Ya Jiang
Dan-Dan Wang
Wei-Jie Zhou
Yu-Wen Zhang
Mei Yang
Jing-Yu Chen
Wei Wei
Journal: Biochemical and Biophysical Research Communications (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CP-25; GRK2; GŒ≤Œ≥; PI3K/AKT signal; Rheumatoid arthritis.
Affiliations: Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Meishan Road 81, Hefei, 230032, China., Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Meishan Road 81, Hefei, 230032, China. Electronic address: .

Abstract:  Objective: This study aims to explore the effect of paeoniflorin-6'-O-benzene sulfonate (CP-25) on the migration of fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA) and the mechanism focused on CXCR4-GŒ≤Œ≥-PI3K/AKT signaling. Methods: Human synovial tissues were collected from RA and osteoarthritis (OA) patients. Immunohistochemistry (IHC) and Western blot were used to detect the protein expression of CXCR4, GRK2, GŒ≤Œ≥, PI3K, p-PI3K, AKT and p-AKT. Transwell was adopted to analyse the migration of fibroblast-like synoviocytes (FLS). Co-immunoprecipitation (Co-IP) and laser scanning confocal microscopy (LSCM) were used to detect the combination of GRK2 and GŒ≤Œ≥, the combination of PI3K and GŒ≤Œ≥. Results: The expression level of CXCR4, GRK2, GŒ≤Œ≥, p-p85 and p-AKT were increased in RA synovial tissue according to the results of IHC and Western blot. In vitro, the migration of FLS was increased after stimulation of CXCL12, inhibition of GŒ≤Œ≥ suppressed the migration and phosphorylation of p85 and AKT induced by CXCL12 in FLS, and CP-25 had the same effect as inhibition of GŒ≤Œ≥. The membrane expression of GRK2, GŒ≤Œ≥, PI3K and the combination of GRK2 and GŒ≤Œ≥, the combination of PI3K and GŒ≤Œ≥ in FLS were increased after the stimulation of CXCL12, and CP-25 had an ability in reducing the membrane expression and the combination of these proteins. Conclusion: Excessive migration of FLS in RA was associated with over-activation of PI3K/AKT signaling, and the activity of GŒ≤Œ≥ was involved in the over-activation of PI3K/AKT. CP-25 down-regulated CXCR4-GŒ≤Œ≥-PI3K/AKT signals by inhibiting GRK2-GŒ≤Œ≥ complex membrane translocation. 

Retracted: No

PubPeer comments:
 Fig. 2A contains two images which appear to overlap, though the brightness of these images is adjusted and not identical.  ,
Effects of agomelatine in rotenone-induced Parkinson's disease in rats
Authors: Hakan Balcƒ±
S Sƒ±rrƒ± Bilge
Mehmet Emin √ñnger
Ayhan Bozkurt
Caner G√ºnaydƒ±n
Bahattin Avcƒ±
Journal: Neuroscience Letters (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Agomelatine; Parkinson's disease; Rat; Rotenone.
Affiliations: Ondokuz Mayƒ±s University, Medical Faculty, Department of Pharmacology, Turkey. Electronic address: ., Ondokuz Mayƒ±s University, Medical Faculty, Department of Biochemistry, Turkey. Electronic address: ., Ondokuz Mayƒ±s University, Medical Faculty, Department of Physiology, Turkey. Electronic address: ., Ondokuz Mayƒ±s University, Medical Faculty, Department of Histology and Embryology, Turkey. Electronic address: .

Abstract:  The effects of melatonin and melatonin analogs in experimental Parkinson's disease (PD) models remain controversial. Agomelatine, a novel analog of melatonin, is both agonists for melatonin-1 and melatonin-2 receptors and antagonist of 5-HT2C receptors. While agomelatine has been commonly used as an anti-depressant and sleep drug, information about effects of agomelatine in PD are still lacking. Male Sprague-Dawley rats (220-260 g) were injected with rotenone (0.5 Œºg, n = 16) or vehicle (1 Œºl DMSO, n = 8) into the left substantia nigra (SN) and ventral tegmental area under stereotaxic surgery. After ten days, the rats were assessed for the confirmation of PD by the rotational test following apomorphine injection (2 mg/kg, i.p.). The confirmed rats were divided into two groups which received daily p.o. agomelatine (40 mg/kg, n = 8) or saline (2 ml/rat, n = 8) for consecutively 18 days. Twenty-four hours after the last drug administration, the rotational test was repeated and motor coordination was assesed just before the decapitation. Brain tissues were taken for biochemical, molecular and histopathological evaluations. Agomelatine treated animals showed augmented apomorphine-induced rotation response and impaired motor coordination compared to the rotenone group. Furthermore, agomelatine treatment significantly induced apoptosis with an increase in caspase-3 expression independent from PARP-1 activation. Agomelatine treatment caused increased protein oxidation levels, in addition to a decrease in neuron number in the striatum. Although we investigated the effects of the agomelatine in the manner of ameliorating the rotenone toxicity in animals, agomelatine exacerbates rotenone-induced toxicity which mimics Parkinson's disease pathology. 

Retracted: No

PubPeer comments:
 Figure 8 duplication with  Behavioural Brain Research 392 (2020) 112692, Figure 6  , 
 Got this kindly comment, Iu2019ll check all the original data carefully and then make a response to the journal. , 
 Thank you for your attention, we fixed the error. ,
Long-term survival of a patient with pancreatic cancer and lung metastasis: A case report and review of literature
Authors: Wen-Wei Yang
Yong-Kun Sun
Hai-Zhen Lu
Lin Yang
Journal: World Journal of Clinical Cases (2021)
Discipline: CLINICAL MEDICINE
Keywords: Apatinib; BAP1 mutation; Case report; PIK3CA mutation; Pancreatic cancer
Affiliations: Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China., Department of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China., Department of Medical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. .

Abstract:  Background: Pancreatic cancer (PC) is a leading cause of cancer-related death, given its poor prognosis and the limited benefits of traditional therapies. As tumors become more genetically disorganized as they progress, genetic mutations might become new markers for us to predict their behavior. Nowadays, many inhibitors can selectively target gene products as a form of targeted therapy, with some showing promise as treatment for various types of cancer. Case summary: We describe a rare case of a PC patient with long-term survival of more than 8 yr. The patient was diagnosed with pancreatic ductal adenocarcinoma (PDAC) with BAP1 and PIK3CA gene mutations and Raf1 fusion and achieved partial response twice after treatment with apatinib in combination with chemotherapy. Conclusion: BAP1, PIK3CA mutations, and Raf1 fusion are rare in PDAC. Patients with these three gene alterations of PDAC may achieve long-term survival with apatinib. Further research in other contexts is needed to determine whether apatinib has ideal efficacy for PC treatment. 

Retracted: No

PubPeer comments:
 According to  (http: https: pubmed.ncbi.nlm.nih.gov 18449193) and    : PIK3CA mutation induces angiogenesis, this could explain that apatinib could make a partial response on this patient. ,
12-O-tetradecanoylphorbol-13-acetate induces Epstein-Barr virus reactivation via NF-kappaB and AP-1 as regulated by protein kinase C and mitogen-activated protein kinase
Authors: K Ikuta
M Tajima
X Gao
T Sairenji
Journal: Virology (2001)
Discipline: MICROBIOLOGY
Keywords: Signaling pathway; Epstein-Barr virus (EBV); 12-O-tetradecanoylphorbol-13-acetate (TPA); protein kinase C (PKC); inducible nitric oxide synthase (iNOS)
Affiliations: Department of Biosignaling, Tottori University, Yonago, 683-8503, Japan.

Abstract:  Signaling pathway components mediating Epstein-Barr virus (EBV) reactivation by 12-O-tetradecanoylphorbol-13-acetate (TPA) were characterized in terms of induction and modification of specific transacting factors. The consequences of protein kinase C (PKC) activation by TPA in inhibiting inducible nitric oxide synthase (iNOS) mRNA expression were analyzed in the EBV-infected gastric epithelial cell line GT38. Spontaneous expression of the EBV BZLF1 gene product ZEBRA became undetectable upon long-term culturing of GT38 cells, while iNOS mRNA expression increased. In such cells the PKC inhibitors 1-(5-isoquinolinesulphonyl)-2,5-dimethylpiperazine (H7) and staurosporine inhibited TPA-induced expression of BZLF1 and BRLF1 and reversed TPA-mediated inhibition of iNOS gene expression. The mitogen-activated protein kinase inhibitor PD98059 inhibited TPA-induced BZLF1 expression. Electrophoretic mobility shift assays demonstrated that transcription factors NF-kappaB and AP-1 were also activated by TPA in a time-dependent manner. The TPA-induced NF-kappaB activation was inhibited by prior treatment of the cells with the NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC). TPA-induced BZLF1 expression was also inhibited by the treatment with PDTC. Northern blot analyses characterized changes in levels of the c-jun and junB expressions of the AP-1 family. These results show that TPA induces EBV reactivation via NF-kappaB and AP-1 and that PKC is an important mediator in regulating gene expression leading to EBV reactivation after TPA treatment of GT38 cells. 

Retracted: No

PubPeer comments:
 there re duplicated figures as marked with green boxes in Fig 7A  ,
Identification of new binding partners of the chemosensory signaling protein GŒ≥13 expressed in taste and olfactory sensory cells
Authors: Xavier Grosmaitre
Esmerina Tili
Claire Fenech
Anna Wiencis
Herv√© Cadiou
Jean-Pierre Montmayeur
Zhenhui Liu
Fabienne Laugerette
Sylvie Grall
Journal: Frontiers in Cellular Neuroscience (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: GOPC; GŒ≥13; MPDZ; PDZ; ZO-1
Affiliations: Chemosensory Perception, Centre des Sciences du Go√ªt et de l'Alimentation, UMR-6265 CNRS, UMR-1324 INRA Dijon, France.

Abstract:  Tastant detection in the oral cavity involves selective receptors localized at the apical extremity of a subset of specialized taste bud cells called taste receptor cells (TRCs). The identification of the genes coding for the taste receptors involved in this process have greatly improved our understanding of the molecular mechanisms underlying detection. However, how these receptors signal in TRCs, and whether the components of the signaling cascades interact with each other or are organized in complexes is mostly unexplored. Here we report on the identification of three new binding partners for the mouse G protein gamma 13 subunit (GŒ≥13), a component of the bitter taste receptors signaling cascade. For two of these GŒ≥13 associated proteins, namely GOPC and MPDZ, we describe the expression in taste bud cells for the first time. Furthermore, we demonstrate by means of a yeast two-hybrid interaction assay that the C terminal PDZ binding motif of GŒ≥13 interacts with selected PDZ domains in these proteins. In the case of the PDZ domain-containing protein zona occludens-1 (ZO-1), a major component of the tight junction defining the boundary between the apical and baso-lateral region of TRCs, we identified the first PDZ domain as the site of strong interaction with GŒ≥13. This association was further confirmed by co-immunoprecipitation experiments in HEK 293 cells. In addition, we present immunohistological data supporting partial co-localization of GOPC, MPDZ, or ZO-1, and GŒ≥13 in taste buds cells. Finally, we extend this observation to olfactory sensory neurons (OSNs), another type of chemosensory cells known to express both ZO-1 and GŒ≥13. Taken together our results implicate these new interaction partners in the sub-cellular distribution of GŒ≥13 in olfactory and gustatory primary sensory cells. 

Retracted: No

PubPeer comments:
 image duplication  Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Role of the A20-TRAF6 axis in lipopolysaccharide-mediated osteoclastogenesis
Authors: Guillaume Mabilleau
Afsie Sabokbar
Daniel Chappard
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bacterial lipopolysaccharide; bone loss; osteoclast precursors; deubiquitinating protease A20; RANKL

Abstract:  Bacterial lipopolysaccharide (LPS) has long been suggested as a potent inducer of bone loss in vivo despite controversial effects on osteoclast precursors. Recently, the role of the deubiquitinating protease A20 in regulating the LPS response in various organs was reported. In the present study, we investigated whether A20 is expressed in osteoclast cultures in response to RANKL or LPS and whether this protein plays a role in osteoclast formation and activation. Human peripheral blood mononuclear cells were cultured in the presence of M-CSF ¬± RANKL ¬± LPS. Although LPS induced the formation of multinucleated TRAP-positive cells expressing OSCAR, cathepsin K, and the calcitonin receptor, these cells were not capable of lacunar resorption. Release of TNF-Œ± was noted in LPS-treated cultures, and the addition of a neutralizing anti-TNF-Œ± antibody abrogated osteoclast formation in these cultures. A20 appeared to be a late-expressed gene in LPS-treated cultures and was associated with TRAF6 degradation and NF-Œ∫B inhibition. Silencing of A20 restored TRAF6 expression and NF-Œ∫B activation and resulted in increased bone resorption in LPS-treated cultures. A20 appeared important in the control of bone resorption and could represent a therapeutic target to treat patients with bone resorption associated with inflammatory diseases. 

Retracted: No

PubPeer comments:
 The two bands share more similarity than expected in Fig.6A and 6B.  ,
Anti-cancer potential of (1,2-dihydronaphtho[2,1-b]furan-2-yl)methanone derivatives
Authors: Kobirul Islam
Kuladip Jana
Abu Taleb Khan
Kunal Pal
Utsab Debnath
Anup Kumar Misra
R Sidick Basha
Journal: Bioorganic & Medicinal Chemistry Letters (2020)
Discipline: CHEMISTRY
Keywords: Anti-cancer; Anti-proliferative; Apoptosis; DBU; Dihydronaphtho[2,1-b]furan.
Affiliations: Bose Institute, Division of Molecular Medicine, P-1/12, C.I.T. Scheme VII M, Kolkata 700054, India; Department of Chemistry, Indian Institute of Technology Guwahati, Guwahati 781 039, India., Bose Institute, Division of Molecular Medicine, P-1/12, C.I.T. Scheme VII M, Kolkata 700054, India., Bose Institute, Division of Molecular Medicine, P-1/12, C.I.T. Scheme VII M, Kolkata 700054, India; Present Address: School of Pharmaceutical Technology, Adamas University, Kolkata - 700126, India., Department of Chemistry, Indian Institute of Technology Guwahati, Guwahati 781 039, India., Bose Institute, Division of Molecular Medicine, P-1/12, C.I.T. Scheme VII M, Kolkata 700054, India. Electronic address: .

Abstract:  A series of 1,2-dihydronaphtho[2,1-b]furan derivatives were synthesized by cyclizing 1-(aryl/alkyl(arylthio)methyl)-naphthalen-2-ol and pyridinium bromides in the presence of 1,8-diazabicyclo[5.4.0]undec-7-ene (DBU) in very good yield. The synthesized compounds were evaluated for their anti-proliferative potential against human triple negative MDA-MB-468 and MCF-7 breast cancer cells and non-cancerous WI-38 cells (lung fibroblast cell) using MTT experiments. Among 21 synthesized compounds, three compounds (3a, 3b and 3 s) showed promising anti-cancer potential and compound 3b was found to have best anti-proliferative activities based on the results of several biochemical and microscopic experiments. 

Retracted: No

PubPeer comments:
 Fig no 3C of the paper ** Folic acid conjugated curcumin loaded biopolymeric gum acacia microsphere for triple negative breast cancer therapy in invitro and invivo model and Fig no. 4 a of  Anti-cancer potential of (1,2-dihydronaphtho[2,1-b]furan-2-yl)methanone derivatives   ,
Overexpression of the anaphase-promoting complex (APC) genes in Nicotiana tabacum promotes increasing biomass accumulation
Authors: Marcelo de Freitas Lima
Adriana S Hemerly
Mariana Carnavale Bottino
N√∫bia Barbosa Eloy
Paulo C G Ferreira
Journal: Molecular biology reports (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: anaphase-promoting complex (APC); plant development; Arabidopsis thaliana; tobacco; biomass
Affiliations: Laborat√≥rio de Biologia Molecular de Plantas, Instituto de Bioqu√≠mica M√©dica, CCS, Cidade Universit√°ria - Ilha do Fund√£o, CEP 21941-902, Rio de Janeiro, RJ, Brazil, .

Abstract:  The anaphase-promoting complex (APC) plays pivotal roles in cell cycle pathways related to plant development. In this study, we present evidence that overproduction of APC10 from Arabidopsis thaliana in tobacco (Nicotiana tabacum) plants promotes significant increases in biomass. Analyzes of plant's fresh and dried weight, root length, number of days to flower and number of seeds of plants overexpressing AtAPC10 verified an improved agronomic performance of the transgenic plants. Detailed analyzes of the leaf growth at the cellular level, and measurements of leaf cell number, showed that AtAPC10 also produce more cells, showing an enhancement of proliferation in these plants. In addition, crossing of plants overexpressing AtAPC10 and AtCDC27a resulted in a synergistic accumulation of biomass and these transgenic plants exhibited superior characteristics compared to the parental lines. The results of the present study suggest that transgenic plants expressing AtAPC10 and AtAPC10/AtCDC27a concomitantly are promising leads to develop plants with higher biomass. 

Retracted: No

PubPeer comments:
 Figure 2A and Figure 2C have some plants with more similarity than expected to represent different genetic backgrounds. Could the authors check please?  ,
Increased expression of claudin‚Ä?2 promotes the metastatic phenotype of human bronchial epithelial cells and is associated with poor prognosis in lung squamous cell carcinoma
Authors: Lemeng Sun
Jiuwei Cui
Liangshu Feng
Journal: Experimental and Therapeutic Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: claudin-12; epithelial-mesenchymal transition; lung squamous cell carcinoma; metastasis; tight junction.
Affiliations: Department of Oncology, Stem Cell and Cancer Center, The First Bethune Hospital, Jilin University, Changchun, Jilin 130021, P.R. China., Department of Neurology and Neuroscience Center, First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.

Abstract:  A prior study by our group using cDNA array analysis identified the tight junction component claudin-12 (CLDN12) to be an upregulated gene in lung squamous cell carcinoma (SqCC) cells compared with normal human bronchial epithelial cells. The present study aimed to explore the effect and underlying molecular mechanism of CLDN12 with regard to the malignant phenotype of SqCC. Firstly, the expression patterns of CLDN12 in SqCC tissues, lung adenocarcinoma tissues and histologically non-neoplastic lung epithelial tissues were investigated by immunohistochemistry and western blotting. Additionally, associations between CLDN12 expression and clinicopathological indicators were examined in patients with SqCC. Furthermore, the impact of CLDN12 on the malignant phenotype of the human bronchial epithelial cell line BEAS-2B in vitro was assessed using the Cell Counting kit-8 assay, Transwell assay and a wound-healing experiment. Western blotting and immunofluorescence were also used to detect the impact of CLDN12 on the epithelial-mesenchymal transition (EMT) of BEAS-2B cells. Tyrosine kinase 2 (Tyk2) RNA interference was further utilized to determine the impact of the Tyk2/signal transducer and activator of transcription 1 (Stat1) signaling pathway on the EMT of BEAS-2B cells. To conclude, it was indicated that the expression of CLDN12 was upregulated in SqCC tissues and was associated with the extent of lymphatic metastasis in patients with SqCC. Furthermore, CLDN12 promoted the EMT of human bronchial epithelial cells in vitro. The findings indicated that the induction of Tyk2/Stat1 signaling appears to be an important mechanism by which CLDN12 promotes the EMT of SqCC cells. 

Retracted: No

PubPeer comments:
 Figure 3D does not match Figure 3C. Figure 4A does not match Figure 4B.   , 
 Dear Dr. Lychnophora Markgravii. Thank you for carefully reading the article and raising the concern about our article published on u201cExperimental and Therapeutic Medicineu201d. In your point of view, figure 3D does not match figure 3C and figure 4A does not match figure 4B. Actually figure 3D and 4B demonstrate statistical data based on multiple experiments, seem not completely accordance with figure 3C and 4A which illustrate just one specific test. We carefully checked and verified that the trends of results are consistent and does not affect the conclusion of the article. Thank you again and look forward to your feedback, suggestions and criticism. ,
MAT2B mediates invasion and metastasis by regulating EGFR signaling pathway in hepatocellular carcinoma
Authors: Fuchen Liu
Zhihui Che
Jun Ying
Wenli Zhang
Dongqin Yang
Qi Zhang
Lijun Wu
Ping Chen
Jun Zhang
Jie Liu
Mengmeng Wu
Bin Lv
Journal: Clinical and experimental medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: EGFR; Hepatocellular carcinoma; Invasion; MAT2B; Migration.
Affiliations: Department of Digestive Diseases of Huashan Hosptial, Fudan University, Shanghai, 200040, China., Fudan University Library, Shanghai, 200433, China., Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China., The Third Department of Hepatic Surgery of Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 200438, China., Department of Digestive Diseases of Huashan Hosptial, Fudan University, Shanghai, 200040, China. .

Abstract:  The poor prognosis of hepatocellular carcinoma (HCC) patients is mainly due to cancer metastasis. Methionine adenosyltransferase 2Œ≤ (MAT2B) encodes a regulatory subunit (Œ≤) for methionine adenosyltransferase. Previous studies reveal that MAT2B provides a growth advantage for HCC, but its role in metastasis is unknown. This study showed that both in the xenograft zebra fish model and in the lung metastasis model in nude mice, the stable inhibition of MAT2B could suppress the metastasis of HCC cancer cells. Silencing of MAT2B in HCC cell lines could remarkably inhibit migration and invasion. By analysis of human phospho-kinase array membranes, we found several differentially expressed proteins, including phosphor-AKT, phospho-EGFR, phospho-Src family, phospho-FAK, phospho-STAT3 and phospho-ERK. We further confirmed the change of these EGFR pathway-related proteins was in accordance with MAT2B expression pattern through immunoblotting test. Finally, we found that MAT2B was overexpressed in HCC caner tissues and correlated with poor prognosis for HCC patients in clinical manifestation. Our study demonstrated that silencing of MAT2B could suppress liver cancer cell migration and invasion through the inhibition of EGFR signaling, which suggested that MAT2B might serve as a new prognostic marker and therapeutic target for HCC. 

Retracted: No

PubPeer comments:
 Many unexpected similarities in figures 2 and 3:   ,
Aberrant whole-brain functional connectivity and intelligence structure in children with primary nocturnal enuresis
Authors: Qiyong Guo
Hongbin Sun
Miao Peng
Fanxing Kong
Bing Yu
Fanxing Meng
Na Liu
Hongwei Ma
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Intelligence structure abnormalities; whole-brain functional connectivity; primary nocturnal enuresis; resting-state functional magnetic resonance imaging; children
Affiliations: Department of Radiology, Shengjing Hospital of China Medical University, Shenyang, China.

Abstract:  Aim: To assess the potential relationship between intelligence structure abnormalities and whole-brain functional connectivity in children with primary nocturnal enuresis (PNE) with resting-state functional magnetic resonance imaging (fMRI) to provide insights into the association between these two seemingly unrelated conditions. Methods: Intelligence testing and fMRI data were obtained from 133 right-handed children, including 67 PNE children (M/F, 39:28; age, 10.5 ¬± 1.2 y) and 66 age-matched healthy controls (M/F, 37:29; age, 10.1 ¬± 1.1 y). All intelligence tests were performed using the China-Wechsler Intelligence Scale for Children (C-WISC). Each subject's full intelligence quotient (FIQ), verbal IQ (VIQ), performance IQ (PIQ), and memory/caution (M/C) factor was measured and recorded. Resting state fMRI scans were performed on a 3.0-T MR scanner and post-processed using REST software. Comparisons of z-score correlation coefficients between distinct cerebral regions were used to identify altered functional connectivity in PNE children. Results: The PNE group had normal FIQ, VIQ, and PIQ values, indicating no significant variation from the control group. However, the M/C factor was significantly lower in the PNE group. Compared to the control group, PNE children exhibited overall lower levels of functional connectivity that were most apparent in the cerebello-thalamo-frontal pathway. The M/C factor significantly correlated with z-scores representing connectivity between Cerebellum_Crus1_L and Frontal_Mid_R. Conclusion: PNE children exhibit intelligence structure imbalance and attention deficits. Our findings suggest that cerebello-thalamo-frontal circuit abnormalities are likely to be involved in the onset and progression of attention impairment in PNE children. 

Retracted: No

PubPeer comments:
 Could the authors please examine the matrices in Figure 1? To my eye, they appear to be the same. ***  ,
MicroRNA 224 Regulates Ion Transporter Expression in Ameloblasts To Coordinate Enamel Mineralization
Authors: Xin Zhou
Yachuan Zhou
Mian Wan
Xuedong Zhou
Bo Gao
Janet Crane
Feifei Sun
Xin Xu
Lei Cheng
Jianxun Sun
Liwei Zheng
Yi Fan
Journal: Molecular and Cellular Biology (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Enamel mineralization; protons; microRNA 224; SLC4A4; CFTR
Affiliations: State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China West China School of Stomatology, Sichuan University, Chengdu, Sichuan, China., State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China., Department of Orthopedics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA., State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China West China School of Stomatology, Sichuan University, Chengdu, Sichuan, China .

Abstract:  Enamel mineralization is accompanied by the release of protons into the extracellular matrix, which is buffered to regulate the pH value in the local microenvironment. The present study aimed to investigate the role of microRNA 224 (miR-224) as a regulator of SLC4A4 and CFTR, encoding the key buffering ion transporters, in modulating enamel mineralization. miR-224 was significantly downregulated as ameloblasts differentiated, in parallel with upregulation of SLC4A4 and CFTR. Overexpression of miR-224 downregulated SLC4A4 and CFTR expression in cultured human epithelial cells. A microRNA luciferase assay confirmed the specific binding of miR-224 to the 3' untranslated regions (UTRs) of SLC4A4 and CFTR mRNAs, thereby inhibiting protein translation. miR-224 agomir injection in mouse neonatal incisors resulted in normal enamel length and thickness, but with disturbed organization of the prism structure and deficient crystal growth. Moreover, the enamel Ca/P ratio and microhardness were markedly reduced after miR-224 agomir administration. These results demonstrate that miR-224 plays a pivotal role in fine tuning enamel mineralization by modulating SLC4A4 and CFTR to maintain pH homeostasis and support enamel mineralization. 

Retracted: No

PubPeer comments:
  , 
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Dynamic restructuring of supported metal nanoparticles and its implications for structure insensitive catalysis
Authors: Charlotte Vogt
Matteo Monai
Anatoly I Frenkel
Maarten Nachtegaal
Raymond R Unocic
Davide Ferri
Esther Groeneveld
Rutger A van Santen
Florian Meirer
Bert M Weckhuysen
Journal: Nature Communications (2021)
Discipline: Multidisciplinary
Keywords: catalysis; structure insensitive reactions; surface reconstruction; Ni metal nanoparticles; particle size
Affiliations: Inorganic Chemistry and Catalysis group, Debye Institute for Nanomaterials Science, Utrecht University, Universiteitsweg 99, 3584 CG, Utrecht, The Netherlands., BASF Nederland B.V., Strijkviertel 61, 3454 PK, De Meern, The Netherlands., Paul Scherrer Institute (PSI), 5232, Villigen PSI, Switzerland., Schuit Institute of Catalysis, Laboratory of Inorganic Chemistry and Catalysis, Eindhoven University of Technology, 5600 MB, Eindhoven, The Netherlands., Center for Nanophase Materials Sciences, Oak Ridge National Laboratory, Oak Ridge, TN, USA., Department of Materials Science and Chemical Engineering, Stony Brook University, Stony Brook, NY, USA., Inorganic Chemistry and Catalysis group, Debye Institute for Nanomaterials Science, Utrecht University, Universiteitsweg 99, 3584 CG, Utrecht, The Netherlands. .

Abstract:  Some fundamental concepts of catalysis are not fully explained but are of paramount importance for the development of improved catalysts. An example is the concept of structure insensitive reactions, where surface-normalized activity does not change with catalyst metal particle size. Here we explore this concept and its relation to surface reconstruction on a set of silica-supported Ni metal nanoparticles (mean particle sizes 1-6 nm) by spectroscopically discerning a structure sensitive (CO2 hydrogenation) from a structure insensitive (ethene hydrogenation) reaction. Using state-of-the-art techniques, inter alia in-situ STEM, and quick-X-ray absorption spectroscopy with sub-second time resolution, we have observed particle-size-dependent effects like restructuring which increases with increasing particle size, and faster restructuring for larger particle sizes during ethene hydrogenation while for CO2 no such restructuring effects were observed. Furthermore, a degree of restructuring is irreversible, and we also show that the rate of carbon diffusion on, and into nanoparticles increases with particle size. We finally show that these particle size-dependent effects induced by ethene hydrogenation, can make a structure sensitive reaction (CO2 hydrogenation), structure insensitive. We thus postulate that structure insensitive reactions are actually apparently structure insensitive, which changes our fundamental understanding of the empirical observation of structure insensitivity. 

Retracted: No

PubPeer comments:
 The similar vibration patterns on the operando FT-IR spectra for different size nanoparticles is quite amazing (Figure 1D), which seems not be from the instrument as these features are not seen under certain gas environments (Figure S14). Can the author explain how this happened?  ,
Expansion of mouse sertoli cells on microcarriers
Authors: Y Wang
S Zhang
J Bi
J Chu
Y Zhuang
X Shi
B Shi
M Guo
Journal: Cell Proliferation (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Sertoli cells; microcarrier bead technology; stirred culture conditions; expansion; differentiation
Affiliations: State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.

Abstract:  Background: Sertoli cells (SCs) have been described as the 'nurse cells' of the testis whose primary function is to provide essential growth factors and create an appropriate environment for development of other cells [for example, germinal and nerve stem cells (NSCs), used here]. However, the greatest challenge at present is that it is difficult to obtain sufficient SCs of normal physiological function for cell transplantation and biological medicine, largely due to traditional static culture parameter difficult to be monitored and scaled up. Objective: Operational stirred culture conditions for in vitro expansion and differentiation of SCs need to be optimized for large-scale culture. Materials and methods: In this study, the culturing process for primary SC expansion and maintaining lack of differentiation was optimized for the first time, by using microcarrier bead technology in spinner flask culture. Effects of various feeding/refreshing regimes, stirring speeds, seed inoculum levels of SCs, and concentrations of microcarrier used for expansion of mouse SCs were also explored. In addition, pH, osmotic pressure and metabolic variables including consumption rates of glucose, glutamine, amino acids, and formation rates of lactic acid and ammonia, were investigated in culture. Results: After 6 days, maximal cell densities achieved were 4.6 x 10(6) cells/ml for Cytodex-1 in DMEM/FBS compared to 4.8 x 10(5) cells/ml in static culture. Improved expansion was achieved using an inoculum of 1 x 10(5) cells/ml and microcarrier concentration of 3 mg/ml at stirring speed of 30 rpm. RESULTS indicated that medium replacement (50% changed everyday) resulted in supply of nutrients and removal of waste products inhibiting cell growth, that lead to maintenance of cultures in steady state for several days. These conditions favoured preservation of SCs in the undifferentiated state and significantly increased their physiological activity and trophic function, which were assessed by co-culturing with NSCs and immunostaining. Conclusion: Data obtained in this study demonstrate the vast potential of this stirred culture system for efficient, reproducible and cost-effective expansion of SCs in vitro. The system has advantages over static culture, which has major obstacles such as lower cell density, is time-consuming and susceptible to contamination. 

Retracted: No

PubPeer comments:
 Figures 1 (different stirring speeds) and 3 (different bead concentrations) appear to be showing the same three panels. Shown with red boxes. Could the authors please check?  ,
Magnetic Properties of Polyvinyl Alcohol and Doxorubicine Loaded Iron Oxide Nanoparticles for Anticancer Drug Delivery Applications
Authors: Misbah Masood
Munir Ahmad
Shahzad Naseem
Muhammad Saeed Akhtar
Amiruddin Shaari
M A Saeed
Saira Riaz
Muhammad Nadeem
Journal: PLoS ONE (2016)
Discipline: Multidisciplinary
Keywords: iron oxide nanoparticles; polyvinyl alcohol; doxorubicin; saturation magnetization; drug delivery
Affiliations: Physics Department, Faculty of Science, Universiti Teknologi Malaysia (UTM), Skudai-81310, Johor, Malaysia., Center of Excellence in Solid State Physics, University of the Punjab, Lahore, 54590, Pakistan., Department of Medical Physics, Institute of Nuclear Medicine and Oncology (INMOL), Lahore, Pakistan., Physics Department, University of Lahore, Lahore, 54600, Pakistan., Divison of Science and Technology, University of Education, Township Campus, Lahore, Pakistan., Department of Oncology, Institute of Nuclear Medicine and Oncology (INMOL), Lahore, Pakistan.

Abstract:  The current study emphasizes the synthesis of iron oxide nanoparticles (IONPs) and impact of hydrophilic polymer polyvinyl alcohol (PVA) coating concentration as well as anticancer drug doxorubicin (DOX) loading on saturation magnetization for target drug delivery applications. Iron oxide nanoparticles particles were synthesized by a reformed version of the co-precipitation method. The coating of polyvinyl alcohol along with doxorubicin loading was carried out by the physical immobilization method. X-ray diffraction confirmed the magnetite (Fe3O4) structure of particles that remained unchanged before and after polyvinyl alcohol coating and drug loading. Microstructure and morphological analysis was carried out by transmission electron microscopy revealing the formation of nanoparticles with an average size of 10 nm with slight variation after coating and drug loading. Transmission electron microscopy, energy dispersive, and Fourier transform infrared spectra further confirmed the conjugation of polymer and doxorubicin with iron oxide nanoparticles. The room temperature superparamagnetic behavior of polymer-coated and drug-loaded magnetite nanoparticles were studied by vibrating sample magnetometer. The variation in saturation magnetization after coating evaluated that a sufficient amount of polyvinyl alcohol would be 3 wt. % regarding the externally controlled movement of IONPs in blood under the influence of applied magnetic field for in-vivo target drug delivery. 

Retracted: No

PubPeer comments:
 Figure 3. * Parts of these plots appear to look repetitive within the same plot or across plots. I have marked some areas that look similar with boxes of the same color without trying to be comprehensive.  , 
 Figure 7C. * Certain areas appear to be visible multiple times within the same photo. I have highlighted some of these with boxes of the same color, without trying to be comprehensive.  ,