摘要
表皮生长因子受体(EGFR)下游的信号通路影响卵巢癌细胞的多种生理活动,包括对自噬的调节。自噬是细胞自我消化的过程,既是细胞在不利生存条件下的自我保护机制,又可以诱导细胞凋亡,并可引起肿瘤耐药。在卵巢癌细胞中,EGFR-Ras-Raf-c-Jun氨基末端激酶(JNK)通路、EGFR-磷脂酰肌醇3激酶(PI3K)-蛋白激酶B(Akt)-哺乳动物雷帕霉素靶蛋白(m TOR)通路和EGFR-两面神激酶(JAK)-信号传导和转录激活因子3(STAT3)通路对自噬既有促进作用,又有抑制作用。近年来,EGFR抑制剂试图通过阻断EGFR信号通路,抑制卵巢癌细胞自噬活动,逆转耐药。综述EGFR下游的3条主要信号通路对卵巢癌细胞自噬的调控作用,以期为卵巢癌的治疗和抗耐药提供新的作用靶点。
EGFR is the epidermal growth factor receptor, and its downstream signaling pathways affect many physiological activities of ovarian cancer cells, including the regulation of autophagy. Autophagy is a process of cell self digestion, which is not only the self protection mechanism of cells under adverse conditions, but also can induce cell death and drug resistance. In ovarian cancer cells, EGFR-Ras-Raf-JNK, EGFR-PI3K-Akt-m TOR, and EGFR-JAK-STAT3 three pathways both promote and inhibit activation of autophagy. In recent years, EGFR inhibitors attempt to block the EGFR signaling pathways and inhibit autophagy activity and reverse drug resistance. The aim of this review is to illustrate the regulatory role of EGFR three main signaling pathways in the regulation of autophagy in ovarian cancer cells, and to provide a new target for ovarian cancer therapy and anti-drug resistance.
出处
《国际妇产科学杂志》
CAS
2017年第2期133-136,共4页
Journal of International Obstetrics and Gynecology
基金
国家自然科学基金(81572551)
关键词
受体
表皮生长因子
信号传导
卵巢肿瘤
自噬
Receptor
epidermal growth factor
Signal transduction
Ovarian neoplasms
Autophagy
作者简介
通信作者：卢美松，E-mail：lumeisong0417@163．com 审校者
