Cha Yong Hoon, Yook Jong In, Kim Hyun Sil, Kim Nam Hee
Department of Oral Pathology, Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, 120-752, Korea.
Arch Pharm Res. 2015 Mar;38(3):313-20. doi: 10.1007/s12272-015-0567-x. Epub 2015 Jan 30.
Aerobic glycolysis is widely accepted as the glucose metabolism for production of biomass such as nucleotides, amino acids, and fatty acids which underlie the anabolic process of cancer cell proliferation. The epithelial-mesenchymal transition (EMT) is a complex cellular mechanism for invasion and metastatic progression in cancer cells. While Snail-mediated EMT regulated by major oncogenic signaling has been well-studied over the last decade, metabolic reprogramming during the EMT has not. In this work, we emphasize the importance of catabolic metabolism for cancer cell survival during cancer cell EMT. Because specific catabolic processes such as autophage and fatty acid oxidation have been well explained, we mainly focus on the general aspects of energy metabolism promoting cancer cell survival under metabolic stress. We also revisit the role of mitochondria in catabolism as oxidative phosphorylation in cancer has long been underestimated. Considering the highly inefficient process of metastatic progression and profound metabolic stress following matrix detachment of solid cancer, catabolic reprogramming during the EMT may play an important role in overcoming metastatic inefficiency of cancer cells.
有氧糖酵解被广泛认为是用于产生生物量（如核苷酸、氨基酸和脂肪酸）的葡萄糖代谢过程，这些生物量是癌细胞增殖合成代谢过程的基础。上皮-间质转化（EMT）是癌细胞侵袭和转移进展的一种复杂细胞机制。在过去十年中，由主要致癌信号调节的Snail介导的EMT已得到充分研究，但EMT过程中的代谢重编程尚未得到充分研究。在这项工作中，我们强调分解代谢对癌细胞EMT过程中癌细胞存活的重要性。由于自噬和脂肪酸氧化等特定分解代谢过程已得到充分解释，我们主要关注在代谢应激下促进癌细胞存活的能量代谢的一般方面。我们还重新审视了线粒体在分解代谢中的作用，因为癌症中的氧化磷酸化长期以来一直被低估。考虑到实体癌基质脱离后转移进展的低效过程和严重的代谢应激，EMT过程中的分解代谢重编程可能在克服癌细胞转移低效方面发挥重要作用。
