文章简介激活肿瘤细胞凋亡途径是临床治疗肿瘤的主要方法之一,但是长期的药物使用导致癌细胞对凋亡诱导产生抵抗。吴乔和林天伟实验室前期合作发现了小分子化合物THPN可以通过TR3介导,以诱导自噬性死亡的方式特异性地抑制黑色素瘤的发生发展,但是对其它肿瘤则没有作用。为了进一步拓展THPN的应用,研究人员深入探讨了阻碍THPN诱导自噬的根本原因和机制。结果表明,在许多非黑色素肿瘤细胞中,Akt2呈现高活性状态,通过 INTRODUCTION Activating tumor cell apoptosis is one of the major clinical approaches to the treatment of cancer, but long-term drug use has led to cancer cell resistance to apoptosis induction. Previous work by Wu Qiao and Lin Tianwei Laboratory found that small molecule compound THPN can specifically inhibit the development of melanoma through TR3-mediated induction of autophagic death, but has no effect on other tumors. In order to further expand the application of THPN, the researchers explored in depth the underlying causes and mechanisms that hinder THPN-induced autophagy. The results show that in many non-melanoma tumor cells, Akt2 showed high activity through