Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, P.R. China.
Department of Orthopedics, the Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China.
Int J Oncol. 2017 Jul;51(1):18-24. doi: 10.3892/ijo.2017.4025. Epub 2017 May 31.
Cellular autophagy and epithelial-mesenchymal transition (EMT) are key events mostly resulted from the interplay of tumor suppressors and oncogenes during cancer progression. The master tumor suppressor p53 may control tumor cell autophagy and EMT through the transcriptional induction of multiple target genes, while the activated oncogene RAS may also play a critical role in regulating mitogenic signaling to tumor cell autophagy and EMT. Although the fundamental functions of p53 and RAS are well understood, the interactive effects of p53 and RAS on autophagy and EMT are still unclear. In this review, we highlight the recent advances in the regulation of autophagy and EMT by p53 and RAS, aiming to explore novel therapeutic targets and biomarkers in cancer treatment and prevention.
细胞自噬和上皮-间充质转化(EMT)是肿瘤进展过程中主要由肿瘤抑制因子和癌基因相互作用产生的关键事件。主肿瘤抑制因子 p53 可能通过多个靶基因的转录诱导来控制肿瘤细胞自噬和 EMT,而激活的癌基因 RAS 也可能在调节肿瘤细胞自噬和 EMT 的有丝分裂信号中发挥关键作用。尽管 p53 和 RAS 的基本功能已经得到很好的理解,但 p53 和 RAS 对自噬和 EMT 的相互作用仍不清楚。在这篇综述中,我们强调了 p53 和 RAS 对自噬和 EMT 的调控的最新进展,旨在探索癌症治疗和预防中的新的治疗靶点和生物标志物。