Cheong Heesun
Comparative Biomedicine Research Branch, Division of Cancer Biology, National Cancer Center, 323 Ilsan-ro, Ilsandong-gu, Goyang, Gyeonggi-do, 410-769, Republic of Korea,
Arch Pharm Res. 2015 Mar;38(3):358-71. doi: 10.1007/s12272-015-0562-2. Epub 2015 Jan 24.
Autophagy is a catabolic process mediated by lysosomal degradation and is a key player in regulating cellular metabolism during cancer progression. Autophagy maintains cellular homeostasis by degrading unnecessary cellular molecules, which also prevents tumorigenesis. Conversely, autophagy also provides nutrients that support malignant tumor growth in advanced tumors. Multiple novel mechanisms have been proposed to explain the tumor-facilitating role of autophagy. Autophagy regulates diverse metabolic pathways that promote tumor proliferation and survival, which are closely associated with oncogenic activators and tumor suppressors. Autophagy has been implicated in cancer cell invasion and metastasis. Accordingly, autophagy has emerged as a tumor-promoting mechanism that facilitates cancer cell growth and survival. Mechanistic studies of autophagy during tumor progression may identify potential targets that can be utilized to disrupt cancer development. Understanding the molecular networks integrating metabolic changes and autophagy in cancer cells could provide novel insights to enhance targeted cancer therapies.
自噬是一种由溶酶体降解介导的分解代谢过程,是癌症进展过程中调节细胞代谢的关键因素。自噬通过降解不必要的细胞分子来维持细胞内稳态,这也可预防肿瘤发生。相反,自噬还为晚期肿瘤中支持恶性肿瘤生长的营养物质提供支持。人们提出了多种新机制来解释自噬的促肿瘤作用。自噬调节多种促进肿瘤增殖和存活的代谢途径,这些途径与致癌激活因子和肿瘤抑制因子密切相关。自噬与癌细胞的侵袭和转移有关。因此,自噬已成为一种促进癌细胞生长和存活的肿瘤促进机制。肿瘤进展过程中自噬的机制研究可能会确定可用于破坏癌症发展的潜在靶点。了解整合癌细胞代谢变化和自噬的分子网络可为增强靶向癌症治疗提供新见解。