STK39 enhances the progression of Cholangiocarcinoma via PI3K/AKT pathway

Xiaopei Hao; Yao Zhang; Yiwei Lu; Guoyong Han; Dawei Rong; Guoqiang Sun; Guangshun Sun; Weiwei Tang; Jindao Wu; Xuehao Wang

doi:10.1016/j.isci.2021.103223

STK39 enhances the progression of Cholangiocarcinoma via PI3K/AKT pathway

iScience. 2021 Oct 6;24(11):103223. doi: 10.1016/j.isci.2021.103223. eCollection 2021 Nov 19.

Authors

Xiaopei Hao¹, Yao Zhang¹, Yiwei Lu¹, Guoyong Han¹, Dawei Rong¹, Guoqiang Sun², Guangshun Sun², Weiwei Tang¹, Jindao Wu^{1

3}, Xuehao Wang¹

Affiliations

¹ Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, Jiangsu, China.
² Department of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
³ State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu, China.

Abstract

Serine/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 by in vivo experiments. 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.

Keywords: Biological sciences; Cancer; Molecular biology.