TRIM59 predicts poor prognosis and promotes pancreatic cancer progression via the PI3K/AKT/mTOR‐glycolysis signaling axis. Issue 2 (6th November 2019)

• Record Type: Journal Article
• Authors: Li, Rongkun; Weng, Li; Liu, Bingyan; Zhu, Lili; Zhang, Xiaoxin; Tian, Guangang; Hu, Lipeng; Li, Qing; Jiang, Shuheng; Shang, Mingyi
• Is Part Of: Journal of cellular biochemistry. Volume 121:Issue 2(2020)
• Page Start: 1986
• Page End: 1997
• Publication Date: 2019-11-06
• Subjects: glycolysis -- metastasis -- pancreatic cancer -- PI3K/AKT/mTOR pathway -- proliferation -- tripartite motif containing 59; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.29433
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Aberrant expression of the tripartite motif containing 59 (TRIM59) has been reported to participate in the development and progression of various human cancers. However, its expression pattern and cellular roles in pancreatic cancer (PC) remains unclear. In our study, we found that TRIM59 expression was significantly increased in PC tissues and was positively correlated with several malignant behaviors and poor overall survival of PC patients based on bioinformatics analysis and immunohistochemistry staining. Functionally, small interfering RNA–mediated TRIM59 depletion inhibited cell proliferation and migration in vitro, while TRIM59 overexpression promoted cell proliferation and migration in vitro and drove tumor growth and liver metastasis in vivo. Mechanically, TRIM59 was found to enhance glycolysis through activating the PI3K/AKT/mTOR pathway, ultimately contributing to PC progression. Taken together, our results demonstrate that TRIM59 may be a potential predictor for PC and promotes PC progression via the PI3K/AKT/mTOR‐glycolysis signaling pathway, which establishes the rationale for targeting the TRIM59‐related pathways to treat PC. Abstract : TRIM59 was upregulated in PC and is associated with advanced clinical features. TRIM59 promoted PC cell proliferation and metastasis by enhancing glycolysis though the PI3K/AKT/mTOR signaling pathway.