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.

已知 Perilipin 2 (Plin2) 在多种人类恶性肿瘤中失调，从而促进癌症进展。近期研究发现Plin2的异常表达与非小细胞肺癌（NSCLC）的不良预后相关。然而，Plin2的具体作用及其潜在机制仍不清楚。本研究发现，Plin2在NSCLC组织中表达较低，其相对较高的表达表明肿瘤体积较大，预后较差。体外实验证明Plin2通过激活AKT/mTOR通路促进NSCLC细胞增殖并抑制自噬。同时，用 AKT 磷酸化启动子或抑制剂处理分别中和了 Plin2 缺失或过度表达对增殖和自噬的影响。体内研究表明Plin2刺激裸鼠皮下NSCLC细胞的肿瘤发生。总的来说，这项研究阐明了 Plin2 的致癌作用及其在 NSCLC 进展中的分子机制，这可能有助于未来的靶向治疗。