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Biochemical and biophysical research communications v.494 no.3/4, 2017년, pp.594 - 601   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

TRIP6 promotes cell proliferation in hepatocellular carcinoma via suppression of FOXO3a

Zhao, Wenhui (BinZhou Medical University, Yantai 264003, China ) ; Dai, Yubin (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) ; Dai, Ting (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) ; Xie, Tian (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) ; Su, Xiaobo (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) ; Li, Jing (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) ; Zhou, Xiang (Department of Microsurgery, Trauma and Hand Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China ) ; Meng, Kewei (Tianjin First Center Hospital, Tianjin 300192, China ) ; Zhao, Xiaohui (GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou 511436, China ) ;
  • 초록  

    Abstract Thyroid hormone receptor-interacting protein 6 (TRIP6), a member of LIM family, acts as an adaptor protein and is overexpressed in several tumor types. However, the clinical significance and biological role of TRIP6 in HCC remains unknown. In our study, we found that TRIP6 was markedly overexpressed in HCC cells and clinical specimens compared with normal hepatocytes and adjacent non-tumor tissues. Immunohistochemical and statistical analysis showed that the expression of TRIP6 significantly correlated with HCC patients' clinical stage and poor survival. Moreover, we demonstrated that overexpressing TRIP6 significantly enhanced, whereas silencing endogenous TRIP6 inhibited, the proliferation and the anchorage-independent growth ability of HCC cells. In addition, overexpression of TRIP6 accelerated, while inhibition of TRIP6 retarded, G1-S phase transition in HCC cells. We further found that overexpression of TRIP6 increased the activation of AKT and suppressed the transactivity of FOXO3a. Meanwhile, overexpression of TRIP6 leaded to the decreased expression of cyclin-dependent kinase inhibitors p21 Cip1 and p27 Kip1 and increased expression of the cell cycle regulator cyclin D1. While silencing TRIP6 triggered the opposite effect. Taken together, these findings showed that TRIP6 plays an important role in promoting HCC cells proliferation and may serve as a novel prognostic biomarker and therapeutic target in HCC. Highlights TRIP6 was upregulated in HCC cells and tissue. TRIP6 expression was correlated with HCC patients’ clinical stage and poor survival. TRIP6 enhanced the proliferation of HCC cells via suppression of FOXO3a. TRIP6 may serve as a novel prognostic biomarker and therapeutic target in HCC.


  • 주제어

    TRIP6 .   HCC .   Proliferation .   FOXO3a.  

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