Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0043320150380030313
Archives of Pharmacal Research
2015 Volume.38 No. 3 p.313 ~ p.320
Catabolic metabolism during cancer EMT
Cha Yong-Hoon

Yook Jong-In
Kim Hyun-Sil
Kim Nam-Hee
Abstract
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.
KEYWORD
Epithelial-mesenchymal transition (EMT), Catabolism, Cancer, Survival
FullTexts / Linksout information
Listed journal information
SCI(E) MEDLINE ÇмúÁøÈïÀç´Ü(KCI)