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Biochemical and biophysical research communication...Biochemical and biophysical research communications 49건

  1. [해외논문]   The zinc form of carnosine dipeptidase 2 (CN2) has dipeptidase activity but its substrate specificity is different from that of the manganese form   SCI SCIE

    Okumura, Nobuaki (Corresponding author. Institute for Protein Research, Osaka University, 3-2, Yamadaoka, Suita, Osaka 565-0871, Japan.) , Takao, Toshifumi
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 484 - 490 , 2017 , 0006-291x ,

    초록

    Abstract Carnosine dipeptidase II (CN2), a metallopeptidase present in the cytosol of various vertebrate tissues, catalyzes the hydrolysis of carnosine and several other dipeptides in the presence of Mn 2+ . Although the metal-binding center of mouse CN2 is also able to associate with Zn 2+ in vitro , it was not known whether the zinc form of CN2 has any enzymatic activity. In the present study, we show that Zn 2+ has a higher affinity for binding to CN2 than Mn 2+ , as evidenced by native mass spectrometry. The issue of whether the zinc form of CN2 has enzymatic activity was also examined using various dipeptides as substrates. The findings indicate that the zinc form of CN2 catalyzes the hydrolysis of several different dipeptides including Leu-His, Met-His and Ala-His at a reaction rate comparable to that for its manganese form. On the other hand, the zinc form of CN2 did not catalyze the hydrolysis of carnosine and several other dipeptides that are hydrolyzed by the manganese form of CN2. Substrate specificity was also examined in HEK293T cells expressing CN2, and the findings indicate that Leu-His, Met-His, but not carnosine, were hydrolyzed in the cell culture. These results suggest that the zinc form of CN2 is an active enzyme, but with a different substrate specificity from that of the manganese form. Highlights Carnosine dipeptidase 2 (CN2) forms a high affinity complex with Zn 2+ . Zn 2+ -CN2 complex has dipeptidase activity. Substrate specificity of Zn 2+ -CN2 is different from that of Mn 2+ -CN2. HEK293T cells expressing CN2 hydrolyze dipeptides like Zn 2+ -CN2.

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  2. [해외논문]   Characterization of overexpression of the alternatively spliced isoform of the protein phosphatase 2A catalytic subunit in cells   SCI SCIE

    Tang, Shen (School of Preclinical medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China ) , Liu, Yuyang (Hunan Provincial Center for Disease Control and Prevention, Changsha, Hunan, 410005, China ) , Wang, Xinhang (Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, China ) , Liang, Ziwei (Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, China ) , Cai, Haiqing (Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, China ) , Mo, Laiming (School of Preclinical medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China ) , Xiao, Deqiang (Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, China ) , Guo, Songchao (Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, China ) , Ouyang, Yiqiang (Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, China ) , Sun, Bin (Guangxi Colleges and Universities Key Lab) , Lu, Cailing , Li, Xiyi
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 491 - 498 , 2017 , 0006-291x ,

    초록

    Abstract PP2Acα2 is a recently discovered PP2Acα alternative splicing isoform that can be induced following serum withdrawal. It shows enhanced binding to immunoglobulin binding protein 1 and is overexpressed in chronic lymphocytic leukemia patients. Current knowledge concerning PP2Acα2 is limited. In this study, we induced and cloned PP2Acα2 from HL-60 cells and human lymphocytes, transfected them into human embryonic kidney 293 cells and constructed a stable overexpression cell line. We found that PP2Acα2 mRNA inhibits expression of its longer isoform PP2Acα mRNA but had no effect on the final protein expression and modification of this longer isoform. Moreover, PP2Acα2-overexpressed cells demonstrated increased expression of IGBP1, activated mTORC1 signaling to reduce basal autophagy and increased anchorage-independent growth. Our study provides new insights into the complex mechanisms of PP2A regulation. Highlights PP2Acα2 mRNA inhibits expression of its longer isoform PP2Acα mRNA. PP2Acα2 overexpression increases expression of IGBP1. PP2Acα2 overexpression activates mTORC1 signaling to reduce basal autophagy. PP2Acα2 overexpression increases anchorage-independent growth.

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  3. [해외논문]   Loss of Ribosomal Protein L24A (RPL24A) suppresses proline accumulation of Arabidopsis thaliana ring zinc finger 1 (atrzf1) mutant in response to osmotic stress   SCI SCIE

    Park, Seung-Hyeon (Department of Plant Biotechnology, Chonnam National University, Gwangju 61186, Republic of Korea ) , Chung, Moon-Soo (Korea Atomic Energy Research Institute, Jeollabuk-do 56212, Republic of Korea ) , Lee, Sungbeom (Korea Atomic Energy Research Institute, Jeollabuk-do 56212, Republic of Korea ) , Lee, Kyeong-Hwan (Department of Rural and Biosystems Engineering, Agricultural Robotics and Automation Research Center, Chonnam National University, Gwangju 61186, Republic of Korea ) , Kim, Cheol Soo (Department of Plant Biotechnology, Chonnam National University, Gwangju 61186, Republic of Korea)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 499 - 503 , 2017 , 0006-291x ,

    초록

    Abstract Proline (Pro) metabolism in plants is involved in various cellular processes mediated during abiotic stress. However, the Pro-regulatory mechanisms are unclear. We used a suppressor mutation technique to isolate novel genes involved in the regulation of Pro metabolism in Arabidopsis . Using atrzf1 as a parental plant for T-DNA tagging mutagenesis, we identified a suppressor mutant, termed proline content alterative 21 ( pca21 ), that displayed reduced Pro contents compared with the atrzf1 under osmotic stress conditions. Genomic Thermal Asymmetric Interlaced (TAIL)-PCR revealed pca21 harbored an inserted T-DNA in the region of At2g36620 that encodes Ribosomal Protein L24A. In general, the pca21 mutant partially suppressed the insensitivity of atrzf1 to osmotic stress and abscisic acid during seed germination and early seedling stage. Additionally, the pca21 mutant had increased MDA content and lower expression of several Pro biosynthesis-related genes than the atrzf1 mutant during drought condition. These results suggest that pca21 acts as partial suppressor of atrzf1 in the osmotic stress response through the Pro-mediated pathway. Highlights PCA21 regulates the proline production of atrzf1 in response to drought. PCA21 suppresses partially the AtRZF1 in response to dehydration and abscisic acid. RPL24A positively involved in Pro accumulation during drought stress.

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  4. [해외논문]   The L1 adhesion molecule normalizes neuritogenesis in Rett syndrome-derived neural precursor cells   SCI SCIE

    Yoo, Myungsik (W. M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, 604 Allison Road, Piscataway, NJ 08845, USA ) , Carromeu, Cassiano (School of Medicine, Department of Pediatrics/Rady Children's Hospital San Diego, Department of Cellular and Molecular Medicine, Stem Cell Program, 9500 Gilman Drive, La Jolla, CA 92093, MC 0695, USA ) , Kwon, Ohyoon (W. M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, 604 Allison Road, Piscataway, NJ 08845, USA ) , Muotri, Alysson (School of Medicine, Department of Pediatrics/Rady Children's Hospital San Diego, Department of Cellular and Molecular Medicine, Stem Cell Program, 9500 Gilman Drive, La Jolla, CA 92093, MC 0695, USA ) , Schachner, Melitta (W. M. Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, 604 Allison Road, Piscataway, NJ 08845, USA)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 504 - 510 , 2017 , 0006-291x ,

    초록

    Abstract Therapeutic intervention is an important need in ameliorating the severe consequences of Rett Syndrome (RTT), a neurological disorder caused by mutations in the X-linked gene methyl-CpG-binding protein-2 (MeCP2). Following previously observed morphological defects in induced pluripotent stem cell (iPSC)-derived neurons obtained from female RTT patients, we hypothesized that transfection with the L1 cell adhesion molecule (L1) could contribute to normalizing a pathological male cell system bearing a nonsense mutation of MeCP2. We found a decreased expression of L1 in RTT iPSCs-derived neural precursor cells (RTT NPCs) and decreased neuritogenesis. Expression of wild-type MeCP2 in RTTNPCs revealed a positive correlation between the levels of MeCP2 and L1, and normalization of cell survival. Expression of L1 in RTTNPCs enhanced neuritogenesis and soma size. Knock-down of MeCP2 in wild type NPCs reduced neuritogenesis. L1 expression is regulated by the MeCP2 promoter. These results suggest that a deficiency in L1 may partially account for RTT phenotypes. Highlights L1 expression is downregulated in RTT NPCs. MeCP2 expression correlates positively with L1 expression levels. MeCP2 and L1 expression in RTT NPCs normalizes their impaired neuritogenesis. MeCP2 expression rescues the reduced substrate adhesion of RTT NPCs. MeCP2 binds to an E-box domain in the human L1 promoter, enhancing transcription.

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  5. [해외논문]   Overexpression of DBC1, correlated with poor prognosis, is a potential therapeutic target for hepatocellular carcinoma   SCI SCIE

    Li, Changcan (Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China ) , Liao, Jianhua (Department of General Surgery, Zhejiang Hospital, Hangzhou 310013, China ) , Wu, Shaohan (Department of General Surgery, The Second Affiliated Hospital of Jiaxing College, Jiaxing 314000, China ) , Fan, Junwei (Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China ) , Peng, Zhihai (Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China ) , Wang, Zhaowen (Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 511 - 517 , 2017 , 0006-291x ,

    초록

    Abstract Deleted in Breast Cancer 1 (DBC1) is a regulatory protein involved in cell metabolism and cancer progression. Nevertheless, the expression and prognostic values of DBC1 in hepatocellular carcinoma (HCC) are still not well understood. The following study investigated the clinical significance and biological function of DBC1 in HCC. Briefly, overexpression of DBC1 at transcriptional and translational levels in human HCC tissues compared to adjacent normal tissues was observed using quantitative real-time polymerase chain reaction (qRT-PCR), western blot (WB) and immunohistochemistry (IHC) approach. Furthermore, upregulated DBC1 was significantly correlated with tumor size (p = 0.005), N stage (p = 0.016), M stage (p = 0.011), tumor differentiation (p in vitro . To conclude, these findings demonstrated that DBC1 was essential in tumorigenesis and proliferation. Moreover, it was identified as a potential therapeutic target for HCC. Highlights DBC1 was upregulated in HCC tissues and cell lines. Overexpression of DBC1 was correlated with clinicopathological parameters in HCC. Overexpression of DBC1 predicts poor disease-free survival (DFS) and overall survival (OS) in HCC. Knockdown of DBC1 inhibits HCC cell lines proliferation.

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  6. [해외논문]   A novel mitochondria-targeted two-photon fluorescent probe for dynamic and reversible detection of the redox cycles between peroxynitrite and glutathione   SCI SCIE

    Sun, Chunlong (School of Biotechnology, Key Laboratory of Instrumental Analysis of Binzhou City, Shandong Provincial Key Laboratory of Eco-environmental Science for Yellow River Delta, Binzhou University, Binzhou 256603, China ) , Du, Wen (School of Biotechnology, Key Laboratory of Instrumental Analysis of Binzhou City, Shandong Provincial Key Laboratory of Eco-environmental Science for Yellow River Delta, Binzhou University, Binzhou 256603, China ) , Wang, Peng (Department of Biomedical Engineering, School of Engineering, China Pharmaceutical University, Nanjing 210009, China ) , Wu, Yang (Research Center of Clinical Oncology, Jiangsu Cancer Hospital, Nanjing 210009, China ) , Wang, Baoqin (School of Biotechnology, Key Laboratory of Instrumental Analysis of Binzhou City, Shandong Provincial Key Laboratory of Eco-environmental Science for Yellow River Delta, Binzhou University, Binzhou 256603, China ) , Wang, Jun (School of Biotechnology, Key Laboratory of Instrumental Analysis of Binzhou City, Shandong Provincial Key Laboratory of Eco-environmental Science for Yel) , Xie, Wenjun
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 518 - 525 , 2017 , 0006-291x ,

    초록

    Abstract Redox homeostasis is important for maintenance of normal physiological functions within cells. Redox state of cells is primarily a consequence of precise balance between levels of reducing equivalents and reactive oxygen species. Redox homeostasis between peroxynitrite (ONOO − ) and glutathione (GSH) is closely associated with physiological and pathological processes, such as prolonged relaxation in vascular tissues and smooth muscle preparations, attenuation of hepatic necrosis, and activation of matrix metalloproteinase-2. We report a two-photon fluorescent probe (TP-Se) based on water-soluble carbazole-based compound, which integrates with organic selenium, to monitor changes in ONOO − /GSH levels in cells. This probe can reversibly respond to ONOO − and GSH and exhibits high selectivity, sensitivity, and mitochondrial targeting. The probe was successfully applied to visualize changes in redox cycles during ONOO − outbreak and antioxidant GSH repair in cells. The probe will lead to significant development on redox events involved in cellular redox regulation. Highlights We report a two-photon fluorescent probe (TP-Se) for optical imaging. TP-Se can monitor reversibly changes in ONOO − /GSH levels in mitochondria. TP-Se will lead to significant development on redox events in cellular redox regulation. Graphical abstract [DISPLAY OMISSION]

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  7. [해외논문]   Role of ROS-TRPM7-ERK1/2 axis in high concentration glucose-mediated proliferation and phenotype switching of rat aortic vascular smooth muscle cells   SCI SCIE

    Yang, Meimei (Corresponding author. Department of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, Yiyuan Street 37, Harbin, 150081 Heilongjiang, PR China. ) , Fang, Jing (Corresponding author. Department of Neurology, The Fourth Clinical Hospital of Harbin Medical University, Yiyuan Street 37, Harbin, 150081 Heilongjiang, PR China.) , Liu, Qingan , Wang, Yan , Zhang, Zhuobo
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 526 - 533 , 2017 , 0006-291x ,

    초록

    Abstract This study investigated the change of transient receptor potential cation channel subfamily M member 7 (TRPM7) expression in rat aortic vascular smooth muscle cells (RAoSMCs) treated with a high concentration of D -glucose (HG) and its role in promoting the proliferative phenotype of RAoSMCs. Chronic exposure to HG increased TRPM7 protein expression and TRPM7 whole-cell currents in RAoSMCs. By contrast, RAoSMC exposure to high concentration of L -glucose and mannital exhibited no such effect. Mechanistically, HG treatment elevated TRPM7 expression by increasing oxidative stress. Data also demonstrated that HG significantly promoted RAoSMC proliferation. In addition, as indicated by the changes of the expression of VSMC differentiation marker molecules, phenotype switching of RAoSMCs occurred during exposing to HG. TRPM7 knockdown partially blocked the HG effect on phenotype switching and RAoSMC proliferation. This phenomenon was achieved through inhibiting the mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK)-ERK signaling pathway. These observations suggest that reactive oxygen species-TRPM7-ERK1/2 axis plays an important role in hyperglycemia-induced development of the proliferative phenotype in RAoSMC. Highlights High concentration of D-glucose (HG) induces phenotype switching of rat aortic vascular smooth muscle cells (RAoSMCs). HG upregulates the expression of transientreceptor potential cation channel subfamily M member 7 (TRPM7) in RAoSMCs. HG-induced oxidative stress is responsible for the upregulation of TRPM7 in RAoSMCs. TRPM7-mediated activation of MEK/ERK pathway is responsible for HG-induced phenotype switching of RAoSMCs.

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  8. [해외논문]   Interleukin-6 deficiency attenuates angiotensin II-induced cardiac pathogenesis with increased myocyte hypertrophy   SCI SCIE

    Chen, Fan (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) , Chen, Dandan (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) , Zhang, Yubin (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) , Jin, Liang (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) , Zhang, Han (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China ) , Wan, Miyang (State Key Laboratory of Natural Medicines, Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210006, China) , Pan, Tianshu , Wang, Xiaochuan , Su, Yuheng , Xu, Yitao , Ye, Junmei
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 534 - 541 , 2017 , 0006-291x ,

    초록

    Abstract Interleukin-6 (IL-6) signaling is critical for cardiomyocyte hypertrophy, while the role of IL-6 in the pathogenesis of myocardium hypertrophy remains controversial. To determine the essential role of IL-6 signaling for the cardiac development during AngII-induced hypertension, and to elucidate the mechanisms, wild-type (WT) and IL-6 knockout (IL-6 KO) mice were infused subcutaneously with either vehicle or AngII (1.5 μg/h/mouse) for 1 week. Immunohistological and serum studies revealed that the extents of cardiac fibrosis, inflammation and apoptosis were reduced in IL-6 KO heart during AngII-stimulation, while cardiac hypertrophy was obviously induced. To investigate the underlying mechanisms, by using myocardial tissue and neonatal cardiomyocytes, we observed that IL-6/STAT3 signaling was activated under the stimulation of AngII both in vivo and in vitro . Further investigation suggested that STAT3 activation enhances the inhibitory effect of EndoG on MEF2A and hampers cardiomyocyte hypertrophy. Our study is the first to show the important role of IL-6 in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6/STAT3 and EndoG/MEF2A pathway that affects cardiac hypertrophy during AngII stimulation. Highlights IL-6 deficiency alleviates cardiac fibrosis during AngII stimulation. IL-6 KO-AngII hearts exhibited decreased inflammation and apoptosis. Cardiac hypertrophy is provoked in IL-6 KO mice under AngII stimulation. IL-6/STAT3 regulates AngII-induced myocyte hypertrophy via EndoG/MEF2A pathway. Graphical abstract Schematic diagram showing the development of cardiomyopathy under the regulation of IL-6 during AngII-stimulation. During AngII stimulation, IL-6 expression increases in cardiomyocytes and activates STAT3. STAT3 phosphorylation promotes its nucleus translocation. On one hand, phosphorylated STAT3 (p-STAT3) facilitates the transcription of genes associated with inflammation; on the other hand, p-STAT3 also strengthens the inhibitory effect of EndoG on MEF2A, resulting in alleviated myocyte hypertrophy. AngII also affects the EndoG-MEF2A signaling pathway by inhibiting EndoG expression, causing increased cardiac hypertrophy. Moreover, AngII promotes myocardium apoptosis via upregulating the ratio of Bax/Bcl-2.Dashed arrows: our hypothesis in the study. [DISPLAY OMISSION]

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  9. [해외논문]   Overexpression of eEF1A1 regulates G1-phase progression to promote HCC proliferation through the STAT1-cyclin D1 pathway   SCI SCIE

    Huang, Jian (Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China ) , Zheng, Chuqian (Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China ) , Shao, Jun (Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China ) , Chen, Leifeng (Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China ) , Liu, Xiuxia (Jiangxi Province Key Laboratory of Molecular Medicine, Nanchang, 330006, China ) , Shao, Jianghua (Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 542 - 549 , 2017 , 0006-291x ,

    초록

    Abstract Hepatocellular carcinoma (HCC) is a common cancer worldwide with an aggressive and highly proliferative activity. Studies had confirmed that HCC cell proliferation is associated with the cell cycle's G1 phase, but the detailed molecular mechanism has not been thoroughly elucidated to date. Eukaryotic translation elongation factor 1A1 (eEF1A1) is an evolutionarily conserved elongation factor protein and is involved in tumor cell proliferation. However, which phase of the cell cycle is regulated by eEF1A1 to influence cell proliferation in HCC and its detailed molecular mechanism remain unclear. In this study, we observed that eEF1A1 influences HCC cell proliferation by regulating the cell cycle's G1 phase. In addition, eEF1A1 influences G1 phase by regulating cyclin D1 expression, promoting HCC cell proliferation both in vitro and in vivo . Moreover, our results indicated that eEF1A1 regulates cyclin D1 expression through STAT1 signaling. STAT1 increases the transcriptional activity of cyclin D1 by binding to the cyclin D1 promoter. Taken together, these findings enabled us to identify a novel mechanism by which eEF1A1 regulates the cell cycle's G1 phase to promote tumor proliferation by regulating cyclin D1 expression through STAT1 signaling in HCC. Highlights eEF1A1 influences HCC proliferation by regulating cell cycle G1 phase. eEF1A1 influences cell cycle G1 phase by regulating cyclin D1 expression. eEF1A1 influences cyclin D1 expression by STAT1 signaling. STAT1 increases cyclin D1 expression by activating the transcriptional activity of cyclin D1.

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  10. [해외논문]   EBV-encoded EBNA1 regulates cell viability by modulating miR34a-NOX2-ROS signaling in gastric cancer cells   SCI SCIE

    Kim, Seung-Mi (Department of Anatomy and Tumor Immunology, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Busan 47392, Republic of Korea ) , Hur, Dae Young (Department of Anatomy and Tumor Immunology, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Busan 47392, Republic of Korea ) , Hong, Seung-Woo (Department of Anatomy and Tumor Immunology, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Busan 47392, Republic of Korea ) , Kim, Ji Hyun (Department of Internal Medicine, Busan Paik Hospital, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Busan 47392, Republic of Korea)
    Biochemical and biophysical research communications v.494 no.3/4 ,pp. 550 - 555 , 2017 , 0006-291x ,

    초록

    Abstract Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) is a viral protein expressed in all EBV-infected cells that induces malignant transformation. EBNA1 is reported to contribute to tumor progression through an increase in reactive oxygen species via nicotinamide adenine dinucleotide phosphate oxidase. However, the underlying molecular mechanism of EBNA1-induced ROS accumulation in gastric cancer is poorly understood. Here, we demonstrated that miR34a regulation by EBNA1 determined cell fate in EBV-infected gastric cancer cells. ROS content and NOX2 expression were higher in EBNA1-expressing SNU719 cells than in EBNA1-nonexpressing SNU638 cells. Downregulation of NOX2 using siRNA technology in SNU719 cells decreased cell viability and ROS content. Regulation of EBNA1 expression in EBV-associated gastric cancers modulated NOX2 expression, ROS content and cell viability. We also showed that upregulation of NOX2 by EBNA1 was mediated by downregulating miRNA34a. Finally, overexpression of miR34a in EBNA1-expressing SNU719 cells induced typical apoptosis, suggesting that reactivation of miR34a in EBNA1-expressing gastric cancer cells could be a strategy for treatment of EBV-infected gastric cancer cells. Highlights ROS content and NOX2 expression are higher in EBV-positive gastric cancer cells relative to EBV-negative gastric cancer cells. Upregulation of NOX2 expression by EBNA1 plays an important role in the cell viability of gastric cancer cells. Modulation of NOX2 expression by EBNA1 is regulated at the transcriptional level via miR34a. Reactivation of miR34a could be a potential anti-cancer strategy in EBV-infected gastric cancer.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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