Lysophosphatidic acid inhibits serum deprivation-induced autophagy in human prostate cancer PC-3 cells.
Lysophosphatidic acid (LPA) is a platelet-enriched bioactive lysophospholipid. By binding to its cognitive G protein-coupled receptors, which are encoded by endothelial differentiation genes (edgs), LPA regulates various cellular activities including proliferation, survival, and migration. Currently, little is known about the influences of LPA on autophagy, a pivotal mechanism for cell survival during conditions of starvation. Herein we present data indicating that LPA attenuates starvation-induced autophagy, by monitoring the percentage of LC3-II, an autophagy indicator, in human prostate PC-3 cells. In addition, by using cells stably expressing EGFP-LC3, LPA is shown to inhibit the formation of autophagosomes in serum-starved conditions. Our results suggest that in these conditions, LPA inhibits autophagy, which might facilitate early cancer development.
Chang
Chi-Lun
CL
Institute of Zoology, National Taiwan University, Taipei, Taiwan.
Liao
Jia-Jun
JJ
Huang
Wei-Pang
WP
Lee
Hsinyu
H
D001343:Autophagy / Q000187:drug effects*; D045744:Cell Line, Tumor; D016895:Culture Media, Serum-Free; D006801:Humans; D008246:Lysophospholipids / Q000494:pharmacology*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000473:pathology; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism
D016895:Culture Media, Serum-Free; D008246:Lysophospholipids; C477012:MAP1LC3A protein, human; D008869:Microtubule-Associated Proteins; D043562:Receptors, G-Protein-Coupled; C032881:lysophosphatidic acid