Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression - Weng, Mei-lin; Chen, Wan-kun; Chen, Xiang-yuan; Lu, Hong; Sun, Zhi-rong; Yu, Qi; Sun, Peng-fei; Xu, Ya-jun; Zhu, Min-min; Jiang, Nan; Zhang, Jin; Zhang, Jian-ping; et al. (Nature communications, 2020)
Keywords: 13/109; 13/2; 13/31; 13/89; 14/34; 14/63; 49; 59; 631/67/1504/1885; 631/67/2327; AKT protein; Animals; Anticancer properties; Antitumor activity; Cancer; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms - metabolism; Colorectal cancer; Colorectal carcinoma; Colorectal Neoplasms - metabolism; Crosstalk; Disease Models, Animal; Down-Regulation; Downstream effects; Farnesyl-diphosphate farnesyltransferase; Farnesyl-Diphosphate Farnesyltransferase - genetics; Farnesyl-Diphosphate Farnesyltransferase - metabolism; Farnesyltransferase; Fasting; Fasting - psychology; Female; Gene expression; Glucose; Glucose metabolism; Glycolysis; Glycolysis - physiology; Humanities and Social Sciences; Humans; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism; Male; Malignancy; Metabolism; Mice, Inbred BALB C; Middle Aged; Molecular modelling; multidisciplinary; Proto-Oncogene Proteins c-akt - metabolism; Science; Science (multidisciplinary); Signal transduction; Signal Transduction - genetics; Signaling; Synergism; TOR protein; TOR Serine-Threonine Kinases - metabolism; Tumor suppressor genes