title: AMP-activated protein kinase supports the NGF-induced viability of human HeLa cells to glucose starvation.
abstract: As an important cellular energy regulation kinase, AMP-activated protein kinase (AMPK) has been demonstrated as a key molecule in the development of tolerance to nutrient starvation. Activation of AMPK includes the phosphorylation of Thr172 of the alpha-subunit. Nerve growth factor (NGF) was originally isolated for its ability to stimulate both survival and differentiation in peripheral neurons, but many investigations have shown that the NGF also plays an important role in survival, growth and invasion of many human cancers. In this study, we used CCK-8 cell viability assay to find that NGF could facilitate the viability of HeLa cells following glucose deprivation while not in glucose-normal control groups. This effect of NGF-induced viability promotion to glucose starvation can be suppressed by Compound C, a specific inhibitor of AMPK. Meanwhile, western blot analysis showed that AMPKalpha1/alpha2 Thr172 phosphorylation level in HeLa cells was up-regulated after NGF treatment under glucose starvation, and Compound C was able to reduce the AMPKalpha1/alpha2 Thr172 phosphorylation level which was up-regulated by NGF in HeLa cells. Taken together, these results indicate that AMP-activated protein kinase supports the NGF-induced viability of human HeLa cells to glucose starvation.
authors.affiliation: State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, 220 Handan Road, 200433 Shanghai, People's Republic of China.
authors.forename: Luo
authors.initials: L
authors.lastname: Ting
authors.forename: Wan
authors.initials: W
authors.lastname: Bo
authors.forename: Ruwei
authors.initials: R
authors.lastname: Li
authors.forename: Xinya
authors.initials: X
authors.lastname: Chen
authors.forename: Yingli
authors.initials: Y
authors.lastname: Wang
authors.forename: Zhou
authors.initials: Z
authors.lastname: Jun
authors.forename: Long
authors.initials: L
authors.lastname: Yu
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D001681:Biological Assay; D002470:Cell Survival / Q000187:drug effects; D005947:Glucose / Q000172:deficiency* / Q000494:pharmacology; D006367:HeLa Cells; D006801:Humans; D051379:Mice; D020932:Nerve Growth Factor / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D047428:Protein Kinase Inhibitors / Q000494:pharmacology
chemical_list: D047428:Protein Kinase Inhibitors; D020932:Nerve Growth Factor; D055372:AMP-Activated Protein Kinases; D005947:Glucose