PI3K/AKT/mTOR通路
蛋白激酶B
生物
癌症研究
糖酵解
细胞生长
转移
胰腺癌
肿瘤进展
信号转导
细胞生物学
癌症
内分泌学
生物化学
遗传学
新陈代谢
作者
Rong-Kun Li,Li Weng,Bingyan Liu,Lili Zhu,Xiaoxin Zhang,Guang-Ang Tian,Li-Peng Hu,Qing Li,Shu‐Heng Jiang,Mingyi Shang
摘要
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.
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