Database : MEDLINE
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[PMID]: 29524886
[Au] Autor:Shan Z; An N; Qin J; Yang J; Sun H; Yang W
[Ad] Address:Clinical Laboratory, Children's Hospital Affiliated to Zhengzhou University, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou City, Henan Province, China.
[Ti] Title:Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/ß-catenin signaling.
[So] Source:Biomed Pharmacother;101:769-776, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Substantial evidence has demonstrated the involvement of long non-coding RNAs (lncRNAs) in the development and progression of colorectal cancer (CRC) via their regulation on cancer cell proliferation, apoptosis, invasion and metastasis pathways. The current study aimed to understand the role of lncRNA Linc00675 in the progression and metastasis of CRC and to identify the potential lncRNA-miRNA interactions and signaling pathways underlying the mechanisms of action of Linc00675 in CRC. Our data firstly demonstrated the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues. Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors. Further studies also showed that overexpression of Linc00675 inhibited the proliferation, invasion and migration of CRC cells. In addition, our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues. More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. Furthermore, we also demonstrated the inhibition of Wnt/ß-catenin signaling in the Linc00675/miR-942 regulated pathway in CRC cells. Taken together, our findings suggested Linc00675 as a potential molecular marker and target for the diagnosis and treatment of CRC and enhanced the current understanding on the mechanisms of action of Linc00675 in CRC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524880
[Au] Autor:Huang D; Jin L; Li Z; Wu J; Zhang N; Zhou D; Ni X; Hou T
[Ad] Address:Department of Neurology, Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou, Guangdong, 510130, China. Electronic address: huang_dehong1@163.com.
[Ti] Title:Isoorientin triggers apoptosis of hepatoblastoma by inducing DNA double-strand breaks and suppressing homologous recombination repair.
[So] Source:Biomed Pharmacother;101:719-728, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Hepatoblastoma (HB) is the most common malignant liver tumor in children. DNA and DNA-associated processes are one of the most important targets of chemotherapeutic agents. Isoorientin (Iso), a natural flavonoid compound, can be extracted from several plant species. The effects of Iso and its molecular mechanisms on hepatic malignancies remain unclear. Herein, the anti-tumor effects of Iso in HB and its underlying mechanisms were explored. We found that Iso significantly inhibited the proliferation of HB cells both in vitro and in vivo. Mechanistic studies showed that Iso triggered cell apoptosis by inducing DNA double-stranded breaks and blocking the initiation process of homologous recombination repair, which was related to the attenuation of ataxia telangiectasia mutated (ATM) activation and inhibiting the binding of phosphorylated ataxia telangiectasia mutated (pATM) and the MRE11-RAD50-NBS1 (MRN) complex. Furthermore, Iso markedly sensitized HB cells to the anti-proliferative effects of the poly ADP-ribose polymerase (PARP) inhibitor olaparib both in vivo and in vitro. Taken together, our study first showed that Iso was a DNA-damage agent, and the combination of Iso with a PARP inhibitor might be a promising strategy for treating HB patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524829
[Au] Autor:Aupperlee MD; Kariagina A; Zaremba N; Basson MD; Schwartz RC; Haslam SZ
[Ad] Address:Breast Cancer and the Environment Research Program, Michigan State University, East Lansing, MI; Department of Physiology, Michigan State University, East Lansing, MI. Electronic address: aupperl4@msu.edu.
[Ti] Title:The Proliferative Response to p27 Down-Regulation in Estrogen Plus Progestin Hormonal Therapy is Lost in Breast Tumors.
[So] Source:Transl Oncol;11(2):518-527, 2018 Mar 07.
[Is] ISSN:1936-5233
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increased proliferation and breast cancer risk has been observed in postmenopausal women receiving estrogen (E) + progestin hormone replacement therapy (HRT). Progestin action is mediated through two progesterone receptor (PR) isoforms, PRA and PRB, with unique transcriptional activity and function. The current study examines hormonal regulation of PR isoforms in the normal postmenopausal human breast and the mechanism by which progestins increase proliferation and breast cancer risk. Archival benign breast biopsies from postmenopausal and premenopausal women, and luminal breast tumor biopsies from postmenopausal women, were analyzed for regulation of PRA and PRB expression by E and E+medroxyprogesterone acetate (MPA). In the postmenopausal breast without HRT, PRA and PRB expression was decreased compared to the premenopausal breast. Both E (n = 12) and E+MPA (n = 13) HRT in the postmenopausal breast were associated with increased PRA and PRB expression, increased nuclear cyclin E expression, and decreased nuclear p27 expression compared to no HRT (n = 16). With E+MPA HRT, there was a further decrease in nuclear p27 and increased Receptor Activator of NF-kappa B Ligand (RANKL) expression compared to E-alone HRT. In luminal breast cancers, E+MPA HRT (n = 6) was also associated with decreased nuclear expression of the cell cycle inhibitor p27 compared to E HRT (n = 6), but was not associated with increased proliferation. These results suggest that p27 mediates progestin-induced proliferation in the normal human breast and that regulation of this proliferative response by E+MPA is lost in breast tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524788
[Au] Autor:Chen GS; Lee SP; Huang SF; Chao SC; Chang CY; Wu GJ; Li CH; Loh SH
[Ad] Address:Division of Orthodontic, Dentofacial Orthopedic & Pediatric Dentistry, Department of Dentistry, School of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei 114, Taiwan.
[Ti] Title:Functional and molecular characterization of transmembrane intracellular pH regulators in human dental pulp stem cells.
[So] Source:Arch Oral Biol;90:19-26, 2018 Mar 06.
[Is] ISSN:1879-1506
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Homeostasis of intracellular pH (pH ) plays vital roles in many cell functions, such as proliferation, apoptosis, differentiation and metastasis. Thus far, Na -H exchanger (NHE), Na -HCO co-transporter (NBC), Cl /HCO exchanger (AE) and Cl /OH exchanger (CHE) have been identified to co-regulate pH homeostasis. However, functional and biological pH -regulators in human dental pulp stem cells (hDPSCs) have yet to be identified. DESIGN: Microspectrofluorimetry technique with pH-sensitive fluorescent dye, BCECF, was used to detect pH changes. NH Cl and Na -acetate pre-pulse were used to induce intracellular acidosis and alkalosis, respectively. Isoforms of pH -regulators were detected by Western blot technique. RESULTS: The resting pH was no significant difference between that in HEPES-buffered (nominal HCO -free) solution or CO /HCO -buffered system (7.42 and 7.46, respectively). The pH recovery following the induced-intracellular acidosis was blocked completely by removing [Na ] , while only slowed (-63%) by adding HOE694 (a NHE1 specific inhibitor) in HEPES-buffered solution. The pH recovery was inhibited entirely by removing [Na ] , while adding HOE 694 pulse DIDS (an anion-transporter inhibitor) only slowed (-55%) the acid extrusion. Both in HEPES-buffered and CO /HCO -buffered system solution, the pH recovery after induced-intracellular alkalosis was entirely blocked by removing [Cl ] . Western blot analysis showed the isoforms of pH regulators, including NHE1/2, NBCe1/n1, AE1/2/3/4 and CHE in the hDPSCs. CONCLUSIONS: We demonstrate for the first time that resting pH is significantly higher than 7.2 and meditates functionally by two Na -dependent acid extruders (NHE and NBC), two Cl -dependent acid loaders (CHE and AE) and one Na -independent acid extruder(s) in hDPSCs. These findings provide novel insight for basic and clinical treatment of dentistry.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524699
[Au] Autor:Zhou YZ; Li CZ; Gao H; Zhang YZ
[Ad] Address:Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing.
[Ti] Title:The effects of Smad3 on ACTH-Secreting Pituitary Adenoma development, cell proliferation, apoptosis, and hormone secretion.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Down-regulation of Smad3 results in the formation of tumors both in vivo and in vitro. However, little is known about the effect of Smad3 on adrenocorticotropic hormone -secreting pituitary adenomas (ACTH-PAs). Our objective was to study the expression and effect of Smad3 in ACTH-PAs and its possible mechanisms. METHODS: Smad3, pSmad3, and Smad2 proteins were detected in samples from 5 normal anterior pituitaries and 18 ACTH-PAs by Western blot and immunohistochemical analysis. Then, Smad3 expression was up-regulated by Smad3-CMV plasmid or down-regulated by small interfering RNA (siRNA) in ACTH tumor cells (AtT-20) in vitro. Cell proliferation, apoptosis, ACTH level, and pSmad3, BCL-2 and POMC protein expression in the AtT-20 cells were measured to investigate the anti-tumor effects of Smad3. RESULTS: Reduced expression of Smad3 and pSmad3, but unchanged Smad2 levels, were found in ACTH-PAs compared to normal pituitaries. In vitro, the over-expression of Smad3 inhibited cell proliferation, promoted cell apoptosis, and decreased ACTH secretion; on the other hand, Smad3 knockdown increased cell proliferation and decreased cell apoptosis but had no significant effect on ACTH secretion. At the same time, over-expression of Smad3 increased pSmad3 but inhibited BCL-2 and POMC protein expression. On the contrary, under-expression of Smad3 inhibited pSmad3 but promoted BCL-2 and POMC protein expression. CONCLUSION: Smad3 is under expressed in ACTH-PAs. Reversing the expression of Smad3 in AtT-20 cells could suppress cell growth, promote tumor apoptosis, and decrease ACTH secretion. Tumor suppression was possibly mediated by the promotion of pSmad3 and the reduction of BCL-2 and POMC expression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524606
[Au] Autor:Zhuang H; Li Q; Zhang X; Ma X; Wang Z; Liu Y; Yi X; Chen R; Han F; Zhang N; Li Y
[Ad] Address:Key Laboratory of Breast Cancer Prevention and Therapy, Laboratory of Cancer Cell Biology, Tianjin Medical University Cancer Institute and Hospital; Research Center of Basic Medical Sciences; Department of Pathogen Biology & Department of Genetics, School of Basic Medical Sciences; Tianjin Medic
[Ti] Title:Downregulation of Glycine Decarboxylase Enhanced Cofilin-mediated Migration in Hepatocellular Carcinoma Cells.
[So] Source:Free Radic Biol Med;, 2018 Mar 07.
[Is] ISSN:1873-4596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Metabolic reprogramming is a hallmark of cancer. Glycine decarboxylase (GLDC), an oxidoreductase, plays an important role in amino acid metabolism. While GLDC promotes tumor initiation and proliferation in non-small cell lung cancer and glioma and it was reported as a putative tumor suppressor gene in gastric cancer, the role of GLDC in hepatocellular carcinoma (HCC) is unknown. In the current study, microarray-based analysis suggested that GLDC expression was low in highly malignant HCC cell lines, and clinicopathological analysis revealed a decrease in GLDC in HCC tumor samples. While the knockdown of GLDC enhanced cancer cell migration and invasion, GLDC overexpression inhibited them. Mechanistic studies revealed that GLDC knockdown increased the levels of reactive oxygen species (ROS) and decreased the ratio of glutathione/oxidized glutathione (GSH/GSSG), which in turn dampened the ubiquitination of cofilin, a key regulator of actin polymerization. Consequently, the protein level of cofilin was elevated, which accounted for the increase in cell migration. The overexpression of GLDC reversed the phenotype. Treatment with N-acetyl-L-cysteine decreased the protein level of cofilin while treatment with H O increased it, further confirming the role of ROS in regulating cofilin degradation. In a tumor xenographic transplant nude mouse model, the knockdown of GLDC promoted intrahepatic metastasis of HCC while GLDC overexpression inhibited it. Our data indicate that GLDC downregulation decreases ROS-mediated ubiquitination of cofilin to enhance HCC progression and intrahepatic metastasis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524503
[Au] Autor:Huang H; Liu L; Li J; Zhu C; Xie X; Ao Y; Wang H
[Ad] Address:Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China; Department of Pharmacy, Wuhan No. 1 Hospital, Wuhan 430022, China.
[Ti] Title:Autophagy as a compensation mechanism participates in ethanol-induced fetal adrenal dysfunction in female rats.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autophagy plays a vital role in embryonic development and cell differentiation. Our previous study demonstrated that prenatal ethanol exposure (PEE) resulted in intrauterine growth retardation (IUGR) and adrenal developmental toxicities in rat offspring. The present study focused on PEE-induced autophagy as an underlying mechanism and its biological significance in female fetal rats. Female fetuses in the PEE group exhibited lower body weights and suffered adrenal structural abnormalities compared to the controls. Cell proliferation was inhibited, the insulin-like growth factor 1 (IGF1) pathway was reduced, and autophagy was activated in the glands of female fetal rats. Ethanol increased the ratio of microtubule-associated protein light chain 3 beta-II (LC3ß-II) to LC3ß-I in vitro, and it reduced cortisol levels in time- and concentration-dependent manners in human adrenocortical carcinoma cells (NCI-H295A). Bafilomycin A1 inhibited autophagy, steroidogenic factor 1 (SF1) protein and steroidogenesis in the present study. Rapamycin with ethanol up-regulated autophagy and SF1 expression and activated steroidogenesis when compared with ethanol alone. In addition, ethanol inhibited IGF1 receptor (IGF1R) and phospho-mTOR (Ser2448) expression in a concentration-dependent manner. These results demonstrate that PEE activated autophagy in fetal adrenal glands, and the underlying mechanism may be associated with inhibition of the IGF1R/phospho-mTOR (Ser2448) pathway. Autophagy may be a compensatory mechanism for the PEE-induced inhibition of fetal adrenal steroidogenesis to maintain fetal adrenal development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524502
[Au] Autor:Nakagawa M; Uno S; Iriyama N; Matsunawa M; Makishima M; Takeuchi J; Tsuboi I; Hatta Y; Takei M
[Ad] Address:Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
[Ti] Title:Combined treatment with benzo[a]pyrene and 1α,25-dihydroxyvitamin D induces expression of plasminogen activator inhibitor 1 in monocyte/macrophage-derived cells.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Benzo[a]pyrene (BaP) is an environmental pollutant found in cigarette smoke and is implicated as a causative agent of tobacco-related diseases, such as arteriosclerosis. In contrast, vitamin D signaling, which is principally mediated by conversion of vitamin D to the active form, 1α,25-dihydroxyvitamin D [1,25(OH) D ], decreases cardiovascular disease risk. However, combined treatment with BaP and 1,25(OH) D enhances BaP toxicity, including BaP-DNA adduct formation. We further investigated the cross-talk between BaP and 1,25(OH) D signaling pathways, and found that combined treatment with these compounds induces mRNA and protein expression of plasminogen activator inhibitor 1 (PAI-1) in monocyte/macrophage-derived THP-1 and U937 cells. Protein synthesis inhibitor treatment did not inhibit induction of the PAI-1 gene (SERPINE1) in these cells. BaP plus 1,25(OH) D induced differentiation markers, inhibited cellular proliferation, and induced apoptosis and oxidative stress in these cells. Reactive oxygen species scavenger treatment suppressed apoptosis but not SERPINE1 induction in cells treated with BaP plus 1,25(OH) D . Thus, combined treatment with BaP and 1,25(OH) D induced SERPINE1 mRNA expression in these cells through a mechanism that does not require de novo protein synthesis or reactive oxygen species production. These findings suggest that induction of the proinflammatory factor PAI-1 plays a role in BaP toxicity. Interestingly, PAI-1 knockdown decreased expression of the cell surface antigen CD14, a monocytic differentiation marker, in THP-1 cells treated with BaP plus 1,25(OH) D . PAI-1 induction may also be related to a function of monocytes/macrophages in response to xenobiotic and vitamin D signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 454171 MEDLINE  
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[PMID]: 29524480
[Au] Autor:Chen L; Zhao Y; Li L; Xie L; Chen X; Liu J; Li X; Jin L; Li X; Ge RS
[Ad] Address:Department of Anesthiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China.
[Ti] Title:Bisphenol A stimulates differentiation of rat stem Leydig cells in vivo and in vitro.
[So] Source:Mol Cell Endocrinol;, 2018 Mar 07.
[Is] ISSN:1872-8057
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Bisphenol A (BPA) is widely used in consumer products and a potential endocrine disruptor linked with sexual precocity. However, its action and underlying mechanisms on male sexual maturation is unclear. In the present study, we used a unique in vivo ethane dimethane sulfonate (EDS)-induced Leydig cell regeneration model that mimics the pubertal development of Leydig cells and an in vitro stem Leydig cell differentiation model to examine the roles of BPA in Leydig cell development in rats. Intratesticular exposure to doses (100 and 1000 pmol/testis) of BPA from post-EDS day 14-28 stimulated Leydig cell developmental regeneration process by increasing serum testosterone level and Leydig cell-specific gene (Lhcgr, Star, Cyp11a1, Hsd3b1, Cyp17a1, Hsd17b3, and Hsd11b1) and their protein expression levels. BPA did not alter serum luteinizing hormone and follicle-stimulating hormone levels as well as the proliferative capacity of Leydig cells in vivo. In vitro study demonstrated that BPA (100 nmol/L) stimulated the differentiation of stem Leydig cells by increasing medium testosterone levels and up-regulating Leydig cell-specific gene (Lhcgr, Cyp11a1, Hsd3b1, Cyp17a1, and Hsd17b3) and their proteins but did not affect their proliferation measured by EdU incorporation. In conclusion, BPA stimulates the differentiation of stem Leydig cells in rat testes, thus possibly causing sexual precocity in the male.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524470
[Au] Autor:Zheng Y; Huang C; Liu F; Lin H; Niu Y; Yang X; Zhang Z
[Ad] Address:Department of Anatomy, Institute of Biomedical Engineering, Second Military Medical University, Shanghai 200433, China.
[Ti] Title:Reactivation of denervated Schwann cells by neurons induced from bone marrow-derived mesenchymal stem cells.
[So] Source:Brain Res Bull;, 2018 Mar 07.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The use of neurons induced from stem cells has been introduced as an effective strategy for promoting peripheral nerve regeneration (PNR). The evolution and role of native denervated Schwann cells (SCs) were often ignored when exploring the mechanisms underlying neural transplantation therapy for PNR. The aim of this study was to understand if following injury, native denervated SCs could be reactivated by transplanting of neurons induced from bone marrow-derived mesenchymal stem cells (NI-BMSCs) to promote PNR. We co-cultured denervated SCs with NI-BMSCs in vitro, tested the proliferation of denervated SCs, and measured the expression and secretion of neurotrophic factors and neural adhesion molecules of the denervated SCs. Concurrently, 48 adult male Sprague-Dawley rats were randomly divided into 4 even groups of 12 rats each: normal group, phosphate-buffered saline (PBS) injection group, BMSCs transplantation group and NI-BMSCs transplantation group. PBS injection and cells transplantation were performed 4 weeks post-injury. After 4 weeks of NI-BMSCs transplantation, the survival of seeded NI-BMSCs was examined, proliferation and ultrastructure of native denervated SCs were detected, and myelination, axonal regeneration and the sciatic functional index measurements were also determinated. Our results demonstrated that NI-BMSCs reactivated denervated SCs both in vitro and in vivo and promoted sciatic nerve regeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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