4.7 Article

THBS4 promotes HCC progression by regulating ITGB1 via FAK/PI3K/AKT pathway

期刊

FASEB JOURNAL
卷 34, 期 8, 页码 10668-10681

出版社

WILEY
DOI: 10.1096/fj.202000043R

关键词

epithelial-mesenchymal transition; FAK; PI3K; AKT pathway; hepatocellular carcinoma development; integrin beta 1; thrombospondin 4

资金

  1. National Science Foundation of China [81602611]
  2. Social Development, Scientific and Technological Research Project of Shannxi Province

向作者/读者索取更多资源

Our research aims to identify the role of thrombospondin 4 (THBS4) in hepatocellular carcinoma (HCC). First, bioinformatic analysis was applied for detection the expression of THBS4 in HCC samples, and qRT-PCR and western blot were performed to explore the expression of THBS4 in HCC tissues and adjacent samples. Next, colony formation assay and cell viability assay were used to assess the function of THBS4 on HCC cells growth while transwell assay and scratch test were for metastasis. Meanwhile Xenograft tumor models were further conducted to verify the function of THBS4 in HCC. As for mechanism in deep, we investigated the influence of THBS4 on epithelial-mesenchymal transition (EMT) development and the interaction between THBS4 and integrin (ITG) family using multiple experiments, including western blot, immunofluorescence and immunoprecipitation (IP). As a result, our research discovered that the overexpression of THBS4 in both HCC patients' tissues and cell lines mediates HCC cells proliferation and metastasis in vitro and in vivo. In-depth, THBS4 regulated EMT progression and interacted with ITG family to modulate FAK/PI3K/AKT pathway. In conclusion, THBS4 as an oncogene interacts with integrin beta 1 (ITGB1) to regulate HCC development via FAK/PI3K/AKT pathway.

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