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  • 标题:STK39 enhances the progression of Cholangiocarcinoma via PI3K/AKT pathway
  • 本地全文:下载
  • 作者:Xiaopei Hao ; Yao Zhang ; Yiwei Lu
  • 期刊名称:iScience
  • 印刷版ISSN:2589-0042
  • 出版年度:2021
  • 卷号:24
  • 期号:11
  • 页码:1-21
  • DOI:10.1016/j.isci.2021.103223
  • 语种:English
  • 出版社:Elsevier
  • 摘要:SummarySerine/threonine kinase 39 (STK39) is overexpressed in various tumor tissues and plays an essential role in tumor progression. In this study, we investigated the clinical value, as well as the potential functions and mechanisms of STK39 in cholangiocarcinoma (CCA). The results showed that STK39 was overexpressed in CCA and negatively associated with the prognosis of patients with CCA. Functionally, STK39 knockdown suppressed cell proliferation, migration, and invasion, while STK39 overexpression facilitated tumor aggressiveness. The tumor-promoting effects of STK39 in CCA were also validated byin vivoexperiments. Mechanistically, RNA-seq analysis identified that STK39 enhanced the progression of CCA by activating PI3K/AKT signaling pathway. Furthermore, overexpression of STK39 could induce gemcitabine resistance in CCA cells. Moreover, the increased expression of STK39 may be mediated by the dysregulation of miR-26a-5p. In summary, STK39 could be served as a valuable prognostic candidate and a potential therapeutic target of CCA.Graphical abstractDisplay OmittedHighlights•STK39 was overexpressed in CCA, negatively associated with the prognosis of patients with CCA•STK39 knockdown suppressed cell proliferation and invasion. STK39 overexpression facilitated tumor aggressiveness•STK39 mediates oncogenic effects on CCA cells by activating the PI3K/AKT signaling pathway•STK39 reduces CCA sensitivity to gemcitabine. Increased expression of STK39 may be mediated by dysregulation of miR-26a-5pBiological sciences; Cancer; Molecular biology
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