PI3K/AKT/mTOR通路
自噬
癌变
生物
癌症研究
蛋白激酶B
肺癌
致癌物
细胞生长
磷酸化
癌症
细胞生物学
信号转导
内科学
细胞凋亡
医学
生物化学
遗传学
作者
Yawei Wang,Ye Hu,Rongjian Xu,Xiangfeng Jin,Wenjie Jiao
标识
DOI:10.1016/j.yexcr.2024.113955
摘要
Perilipin 2 (Plin2) is known to be dysregulated in several human malignancies, which facilitates cancer progression. Recent studies have found that the abnormal expression of Plin2 is associated with poor prognosis of non-small cell lung cancer (NSCLC). However, the specific role of Plin2 and its underlying mechanism remain unclear. This study revealed that Plin2 expression was low in NSCLC tissues, and its relatively higher expression indicated larger tumor size and poorer prognosis. In vitro experiments proved that Plin2 promoted NSCLC cellular proliferation and inhibited autophagy by activating the AKT/mTOR pathway. Meanwhile, treatment with the AKT phosphorylation promoter or inhibitor neutralized the influence of Plin2 depletion or over-expression on proliferation and autophagy, respectively. In vivo study showed that Plin2 stimulated subcutaneous tumorigenesis of NSCLC cells in nude mice. Collectively, this study clarified the carcinogenic role of Plin2 and its molecular mechanism in NSCLC progression, which may facilitate a targeted therapy in the future.
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