ASF1A regulates H4Y72 phosphorylation and promotes autophagy in colon cancer cells via a kinase activity. Issue 1 (4th December 2019)

• Record Type: Journal Article
• Authors: Qiu, Fei; Wang, Yun; Chu, Xianqun; Wang, Jing
• Is Part Of: Artificial cells, nanomedicine, and biotechnology. Volume 47:Issue 1(2019)
• Page Start: 2754
• Page End: 2763
• Publication Date: 2019-12-04
• Subjects: Colon cancer -- histone modification -- ASF1A -- H4Y72ph -- autophagy; Artificial cells -- Periodicals; Nanotechnology -- Periodicals; Blood substitutes -- Periodicals; Tissue engineering -- Periodicals; Molecules -- Periodicals; Biotechnology -- Periodicals; 615.39
• DOI: 10.1080/21691401.2019.1617725
• Languages: English
• ISSNs: 2169-1401

Abstract

Abstract: Colon cancer is one of the most malignant cancers. Histone modification is closely related to tumour development. Our study explored the functions of anti-silencing function 1A (ASF1A) on H4 Y72ph in colon cancer cells. Colon cancer cell lines and clinical specimens were obtained and/or transfected with full length ASF1A or interference mRNA to mimic or silence of ASF1A expression. Immunoprecipitation and GST pull down was used to target targeting ASF1A or H4 Y72ph . Cells were transfected with H4 WT - or H4 Y72F -expressing. An in vitro kinase activity assay was set to determine whether ASF1A could phosphorylate H4. The severity of autophagy was measured by detecting number of autophagosomes, number of EGFP-LC3, LC3-II/I, percentage of degradation and expression of autophagy associated gene (ATG). ASF1A positively regulated H4 Y72ph ; Immunoprecipitation assay and GST pull down results showed that ASF1A interacted directly with H4. In addition, ASF1A silence inhibited autophagosomes number, EGFP-LC3 number, LC3-II/I, percentage of degradation and ATG expression. Moreover, H4 Y72F impaired the promoting autophagy effects of ASF1A. The ASF1A-H4 Y72ph axis promoted colon cancer autophagy via transcriptional regulation of ATG genes. ASF1A regulated H4 Y72ph and promotes autophagy in colon cancer cells via a kinase activity through regulation of ATG.