Livin Regulates H2A.X Y142 Phosphorylation and Promotes Autophagy in Colon Cancer Cells via a Novel Kinase Activity

• Published in: Frontiers in oncology Vol. 9; p. 1233
• Main Authors: Ge, Yang, Liu, Bao-Lin, Cui, Jun-Peng, Li, Shu-Qiang
• Format: Journal Article
• Language: English
• Published: Switzerland 14.11.2019
• Subjects: autophagy; colon cancer cells; phosphorylation; Livin; H2A.X
• ISSN: 2234-943X; 2234-943X
• DOI: 10.3389/fonc.2019.01233

To investigate Livin-mediated regulation of H2A.X phosphorylation via a novel kinase activity and its effect on autophagy in colon cancer cells. The interaction between Livin and H2A.X was tested by immunoprecipitation. H2A.X-/- HCT116 cells were transfected with human influenza hemagglutinin (HA)-tagged WT or Y142F phospho-dead mutantH2A.X plasmids. GST-tagged recombinant Livin protein was used to perform pull-down experiment and kinase assay. H2A.X-/-Livin+/+ SW480 cells were co-transfected with H2A.X /H2A.X plasmid and LC3 EGFP-tagged plasmid to explore whether H2A.X was involved in Livin-mediated autophagy induced by starvation in colon cancer cells. Co-immunoprecipitation studies confirmed that Livin interacted with H2A.X and that it was phosphorylation dependent. kinase assay confirmed that Livin could phosphorylate H2A.X. Knockdown of Livin (Livin-/-) in SW480 cells or HCT116 cells canceled the starvation-induced autophagy in colon cancer cells; H2A.X-/-Livin+/+ SW480 cells transfected with H2A.X activated autophagy induced by starvation while cells transfected with H2A.X had no significant difference; Livin-H2A.X axis activated autophagy in colon cancer cells through transcriptionally regulating and . Livin promotes autophagy in colon cancer cells via regulating the phosphorylation of H2A.X .