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    Differential MicroRNA Expression Between Gastric Cancer Tissue and Non-cancerous Gastric Mucosa According to Helicobacter pylori Status

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    https://www.riss.kr/link?id=A103549465

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Background: MicroRNAs (miRNAs) are key post-translational mechanisms which can regulate gene expression in gastric carcinogenesis. To identify miRNAs responsible for gastric carcinogenesis, we compared expression levels of miRNAs between gastric cancer tissue and non-cancerous gastric mucosa according to Helicobacter pylori status.
    Methods: Total RNA was extracted from the cancerous regions of formalin-fixed, paraffin-embedded tissues of H. pylori-positive (n =8) or H. pylori-negative (n = 8) patients with an intestinal type of gastric cancer. RNA expression was analyzed using a 3,523 miRNA profiling microarray based on the Sanger miRBase. Validation analysis was performed using TaqMan miRNA assays for biopsy samples from 107 patients consisted of control and gastric cancer with or without H. pylori. And then, expression levels of miRNAs were compared according to subgroups.
    Results: A total of 156 miRNAs in the aberrant miRNA profiles across the miRNA microarray showed differential expression (at least a 2-fold change, P < 0.05) in cancer tissue, compared to noncancerous mucosa in both of H. pylori-negative and -positive samples. After 10 promising miRNAs were selected, validations by TaqMan miRNA assays confirmed that two miRNAs (hsa-miR-135b-5p and hsa-miR-196a-5p) were significantly increased and one miRNA (hsa-miR-145-5p) decreased in cancer tissue compared to non-cancerous gastric mucosa at H. pylori-negative group. For H. pylori-positive group, three miRNAs (hsa-miR-18a-5p, hsa-miR-135b-5p, and hsa-miR-196a-5p) were increased in cancer tissue. hsa-miR-135b-5p and hsa-miR-196a-5p were increased in gastric cancer in both of H. pylori-negative and -positive.
    Conclusions: miRNA expression of the gastric cancer implies that different but partially common gastric cancer carcinogenic mechanisms might exist according to H. pylori status.
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    Background: MicroRNAs (miRNAs) are key post-translational mechanisms which can regulate gene expression in gastric carcinogenesis. To identify miRNAs responsible for gastric carcinogenesis, we compared expression levels of miRNAs between gastric cance...

    Background: MicroRNAs (miRNAs) are key post-translational mechanisms which can regulate gene expression in gastric carcinogenesis. To identify miRNAs responsible for gastric carcinogenesis, we compared expression levels of miRNAs between gastric cancer tissue and non-cancerous gastric mucosa according to Helicobacter pylori status.
    Methods: Total RNA was extracted from the cancerous regions of formalin-fixed, paraffin-embedded tissues of H. pylori-positive (n =8) or H. pylori-negative (n = 8) patients with an intestinal type of gastric cancer. RNA expression was analyzed using a 3,523 miRNA profiling microarray based on the Sanger miRBase. Validation analysis was performed using TaqMan miRNA assays for biopsy samples from 107 patients consisted of control and gastric cancer with or without H. pylori. And then, expression levels of miRNAs were compared according to subgroups.
    Results: A total of 156 miRNAs in the aberrant miRNA profiles across the miRNA microarray showed differential expression (at least a 2-fold change, P < 0.05) in cancer tissue, compared to noncancerous mucosa in both of H. pylori-negative and -positive samples. After 10 promising miRNAs were selected, validations by TaqMan miRNA assays confirmed that two miRNAs (hsa-miR-135b-5p and hsa-miR-196a-5p) were significantly increased and one miRNA (hsa-miR-145-5p) decreased in cancer tissue compared to non-cancerous gastric mucosa at H. pylori-negative group. For H. pylori-positive group, three miRNAs (hsa-miR-18a-5p, hsa-miR-135b-5p, and hsa-miR-196a-5p) were increased in cancer tissue. hsa-miR-135b-5p and hsa-miR-196a-5p were increased in gastric cancer in both of H. pylori-negative and -positive.
    Conclusions: miRNA expression of the gastric cancer implies that different but partially common gastric cancer carcinogenic mechanisms might exist according to H. pylori status.

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    참고문헌 (Reference)

    1 Baum B, "Transitions between epithelial and mesenchymal states in development and disease" 19 : 294-308, 2008

    2 Noto JM, "The role of microRNAs in Helicobacter pylori pathogenesis and gastric carcinogenesis" 1 : 21-, 2012

    3 Willis BC, "TGF-beta-induced EMT: mechanisms and implications for fibrotic lung disease" 293 : L525-L534, 2007

    4 Shin CM, "Role of Helicobacter pylori infection in aberrant DNA methylation along multistep gastric carcinogenesis" 101 : 1337-1346, 2010

    5 Haykal S, "Re: moving towards in situ tracheal regeneration: the bionic tissue engineered transplantation approach. J. Cell. Mol. Med. Vol. 14, No. 7, 2010, pp. 1877-1889" 15 : 24-25, 2011

    6 Chen C, "MicroRNA-196:critical roles and clinical applications in development and cancer" 15 : 14-23, 2011

    7 Chen YJ, "MicroRNA-18a modulates P53 expression by targeting IRF2 in gastric cancer patients" 31 : 155-163, 2016

    8 Matsushima K, "MicroRNA signatures in Helicobacter pylori-infected gastric mucosa" 128 : 361-370, 2011

    9 Glud M, "MicroRNA expression in melanocytic nevi: the usefulness of formalin-fixed, paraffin-embedded material for miRNA microarray profiling" 129 : 1219-1224, 2009

    10 Wu WK, "MicroRNA dysregulation in gastric cancer: a new player enters the game" 29 : 5761-5771, 2010

    1 Baum B, "Transitions between epithelial and mesenchymal states in development and disease" 19 : 294-308, 2008

    2 Noto JM, "The role of microRNAs in Helicobacter pylori pathogenesis and gastric carcinogenesis" 1 : 21-, 2012

    3 Willis BC, "TGF-beta-induced EMT: mechanisms and implications for fibrotic lung disease" 293 : L525-L534, 2007

    4 Shin CM, "Role of Helicobacter pylori infection in aberrant DNA methylation along multistep gastric carcinogenesis" 101 : 1337-1346, 2010

    5 Haykal S, "Re: moving towards in situ tracheal regeneration: the bionic tissue engineered transplantation approach. J. Cell. Mol. Med. Vol. 14, No. 7, 2010, pp. 1877-1889" 15 : 24-25, 2011

    6 Chen C, "MicroRNA-196:critical roles and clinical applications in development and cancer" 15 : 14-23, 2011

    7 Chen YJ, "MicroRNA-18a modulates P53 expression by targeting IRF2 in gastric cancer patients" 31 : 155-163, 2016

    8 Matsushima K, "MicroRNA signatures in Helicobacter pylori-infected gastric mucosa" 128 : 361-370, 2011

    9 Glud M, "MicroRNA expression in melanocytic nevi: the usefulness of formalin-fixed, paraffin-embedded material for miRNA microarray profiling" 129 : 1219-1224, 2009

    10 Wu WK, "MicroRNA dysregulation in gastric cancer: a new player enters the game" 29 : 5761-5771, 2010

    11 Zhang Z, "MicroRNA and signaling pathways in gastric cancer" 21 : 305-316, 2014

    12 Jiang SB, "Micro-RNA-145-5p inhibits gastric cancer invasiveness through targeting N-cadherin and ZEB2 to suppress epithelial-mesenchymal transition" 9 : 2305-2315, 2016

    13 Rossi AF, "Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection" 18 : 1444-1458, 2016

    14 Nordenstedt H, "Helicobacter pylori-negative gastritis: prevalence and risk factors" 108 : 65-71, 2013

    15 Yoon H, "Helicobacter pylori-negative gastric cancer in South Korea: incidence and clinicopathologic characteristics" 16 : 382-388, 2011

    16 Kim N, "Helicobacter pylori infection and development of gastric cancer in Korea:long-term follow-up" 42 : 448-454, 2008

    17 Belair C, "Helicobacter pylori and gastric cancer: possible role of microRNAs in this intimate relationship" 15 : 806-812, 2009

    18 Lee DG, "Helicobacter pylori CagA promotes Snail-mediated epithelial-mesenchymal transition by reducing GSK-3 activity" 5 : 4423-, 2014

    19 Jae Kwan Jun, "Effectiveness of the Korean National Cancer Screening Program in Reducing Gastric Cancer Mortality" Elsevier BV 152 (152): 1319-1328.e7, 2017

    20 장훈, "Different MicroRNA Expression Levels in Gastric Cancer Depending on Helicobacter pylori Infection" 거트앤리버 발행위원회 9 (9): 188-196, 2015

    21 Seiji Shiota, "Clinical Manifestations of Helicobacter pylori –Negative Gastritis" Elsevier BV 15 (15): 1037-1046.e3, 2017

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    학술지 이력

    학술지 이력
    연월일 이력구분 이력상세 등재구분
    2022 평가 재인증평가 신청대상 (재인증)
    2019-01-01 등재 등재학술지 선정 (계속평가) KCI등재
    2018-12-01 등재 등재후보로 하락 (계속평가) KCI등재후보
    2015-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2013-10-14 학술지명변경 외국어명 : Cancer Prevention Research -> Journal of Cancer Prevention KCI등재
    2012-10-15 학회명변경 영문명 : Korean Association of Cancer Prevention -> Korean Society of Cancer Preveniton KCI등재
    2011-04-04 학술지명변경 외국어명 : Journal of Korean Association of Cancer Prevention -> Cancer Prevention Research KCI등재
    2011-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2008-01-01 등재 등재학술지 선정 (등재후보2차) KCI등재
    2007-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2005-01-01 등재 등재후보학술지 선정 (신규평가) KCI등재후보
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    기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
    2016 0.22 0.22 0.18
    KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
    0.15 0.12 0.405 0.13
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