Fulda Simone
Institute for Experimental Cancer Research in Pediatrics, Goethe-University Frankfurt, Frankfurt, Germany.
German Cancer Consortium (DKTK), Partner Site Frankfurt, Frankfurt, Germany.
Front Oncol. 2017 Jun 15;7:128. doi: 10.3389/fonc.2017.00128. eCollection 2017.
Autophagy represents a catabolic program involved in the degradation of cellular components lysosomes. It serves to mitigate cellular stress and to provide metabolic precursors especially upon starvation. Thereby, autophagy can support the survival of cancer cells. In addition, there is now convincing evidence showing that under certain conditions autophagy can also foster cell death. This dual function of autophagy is also relevant upon anticancer treatment, as many chemotherapeutic agents engage autophagy. A better understanding of the molecular mechanisms that are critical for mediating autophagic cell death in cancer cells will be instrumental to selectively interfere with this cellular program in order to increase the cancer cell's response to cytotoxic drugs. This review illustrates how anticancer drug-induced autophagy is involved in mediating cell death.
自噬是一种参与细胞成分向溶酶体降解的分解代谢程序。它有助于减轻细胞应激，并在饥饿时提供代谢前体。因此，自噬可以支持癌细胞的存活。此外，现在有令人信服的证据表明，在某些情况下自噬也能促进细胞死亡。自噬的这种双重功能在抗癌治疗中也很重要，因为许多化疗药物都能引发自噬。更好地理解介导癌细胞自噬性细胞死亡的关键分子机制，将有助于选择性地干扰这一细胞程序，从而增强癌细胞对细胞毒性药物的反应。这篇综述阐述了抗癌药物诱导的自噬如何参与介导细胞死亡。
