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      LINC00665 induces gastric cancer progression through activating Wnt signaling pathway

      한글로보기

      https://www.riss.kr/link?id=O113187149

      • 저자
      • 발행기관
      • 학술지명
      • 권호사항
      • 발행연도

        2020년

      • 작성언어

        -

      • Print ISSN

        0730-2312

      • Online ISSN

        1097-4644

      • 등재정보

        SCI;SCIE;SCOPUS

      • 자료형태

        학술저널

      • 수록면

        2268-2276   [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]

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        • 성균관대학교 중앙학술정보관  
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        • 충남대학교 중앙도서관  
        • 한양대학교 백남학술정보관  
        • 이화여자대학교 중앙도서관  
        • 고려대학교 도서관  
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      부가정보

      다국어 초록 (Multilingual Abstract)

      Long noncoding RNAs (lncRNAs) are recently recognized as noteworthy regulators of different tumors, counting gastric cancer (GC). Lately, long intergenic noncoding RNA (LINC) 00665 has been verified to display significant parts in several cancers. Be ...

      Long noncoding RNAs (lncRNAs) are recently recognized as noteworthy regulators of different tumors, counting gastric cancer (GC). Lately, long intergenic noncoding RNA (LINC) 00665 has been verified to display significant parts in several cancers. Be that as it may, its role and mechanism in GC movement still stay uninvestigated. As of now, we observed LINC00665 was obviously GC cells (MKN28, BGC‐823, SGC7‐901, AGS, HGC‐27) in comparison to GES‐1 cells, which was identified as human normal gastric epithelial cells. Then, LINC00665 was obviously downregulated in GC cells including AGS and BGC‐823 cells. Loss of LINC00665 greatly repressed AGS and BGC‐823 cell survival and cell expansion. Moreover, GC cell apoptosis was significantly induced by the loss of LINC00665. For another, we found that the GC cell cycle was also captured in G1 and G2 phases. The experiments on cell migration and invasion indicated that knockdown of LINC00665 restrained GC cell migration and invasion. Modifications in Wnt signaling are closely associated with the development of cancers. Here, we found that Wnt signaling was significantly inactivated by the silence of LINC00665 in GC cells. β‐catenin and cyclinD1 were restrained whereas GSK‐3β was induced by the inhibition of LINC00665 in GC cells. Furthermore, we confirmed the impact of LINC00665 in vivo using xenograft models. Taken these together, we indicated that LINC00665 could function as a novel biomarker in GC progression.
      We found that Wnt signaling was significantly inactivated by the silence of LINC00665 in gastric cancer (GC) cells.β‐catenin and cyclinD1 was restrained whereas GSK‐3β was induced by the inhibition of LINC00665 in GC cells.We indicated that LINC00665 could function as a novel biomarker in GC progression.

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