Y-box binding protein 1 (YBX1) is involved in the development of multiple types of tumors. However, the relationship between YBX1 and autophagy in non-small cell lung cancer (NSCLC) remains unclear. In this study, we analyzed the expression and clinical significance of YBX1 and markers of autophagy (LC3I/II) in NSCLC and examined their roles in regulating sensitivity to cisplatin in NSCLC. The retrospective analysis of patients with NSCLC indicated that YBX1 was positively correlated with autophagy. Increased levels of YBX1 or autophagy also observed in NSCLC cells compared with those in 16HBE cells. Compared to the controls, the knockdown of YBX1 expression suppressed autophagy, increased drug sensitivity and promoted apoptosis in response to cisplatin in NSCLC cells by targeting the p110β promoter and inhibiting p110β/Vps34/beclin1 signaling pathways. We also demonstrated in an in vivo study that the overexpressed YBX1 effectively increased NSCLC growth and progression and decreased the sensitivity to cisplatin by inducing autophagy in a xenograft tumor model, and these effects were concomitant with the increasing of p110β and beclin1 expression. Collectively, these results show that YBX1 plays an essential role in autophagy in NSCLC.

Y-box 结合蛋白 1 (YBX1) 参与多种类型肿瘤的发生。然而，YBX1 与非小细胞肺癌 (NSCLC) 中自噬之间的关系仍不清楚。在本研究中，我们分析了 YBX1 和自噬标志物 (LC3I/II) 在 NSCLC 中的表达和临床意义，并探讨了它们在调节 NSCLC 顺铂敏感性中的作用。 NSCLC患者的回顾性分析表明YBX1与自噬呈正相关。与 16HBE 细胞相比，NSCLC 细胞中 YBX1 或自噬水平也有所增加。与对照组相比，YBX1 表达的敲低通过靶向 p110β 启动子并抑制 p110β/Vps34/beclin1 信号通路，抑制了 NSCLC 细胞中顺铂的自噬，增加了药物敏感性并促进了细胞凋亡。我们还在一项体内研究中证明，过表达的 YBX1 通过在异种移植肿瘤模型中诱导自噬，有效增加 NSCLC 的生长和进展，并降低对顺铂的敏感性，并且这些作用与 p110β 和 beclin1 表达的增加相伴随。总的来说，这些结果表明 YBX1 在 NSCLC 的自噬中发挥重要作用。