- VernacularTitle:脂肪量和肥胖相关蛋白FTO调控IFIT2促进肝细胞癌发生发展
- Author:
Lan LAN
1
;
Zixue XUAN
;
Jinying JIANG
Author Information
- Keywords: FTO; IFIT2; hepatocellular carcinoma; transcriptome sequencing; HepG2; m6A
- From: Acta Universitatis Medicinalis Anhui 2024;59(5):834-839
- CountryChina
- Language:Chinese
- Abstract: Objective To study the molecular mechanism of fat mass and obesity-associated protein (FTO) regula-ting hepatocellular carcinoma (HCC).Methods HepG2 cells of knock-down FTO were constructed, HepG2 cells of knock-down FTO and HepG2 cells were collected, and high-throughput sequencing was performed using Illumina Hiseq platform to screen the gene expression differences between the two groups.Through GO and KEGG enrich-ment analysis of these differential genes, FTO regulatory pathways were studied and downstream target genes of FTO were screened.The role of FTO downstream target gene in HCC was revealed by bioinformatic analysis and cell ex-periments.Results Transcriptome sequencing showed that386 genes were differentially expressed between HepG2 cells of knock-down FTO and HepG2 cells, and they were involved in biological processes such as response to inter-feron-gamma.The expression of IFIT2, one of the most responsive interferon-stimulating genes, was up-regulated after FTO knockdown.Potential m6 A methylation occurred at multiple sites of IFIT2.The survival of HCC patients with high expression of IFIT2 was significantly prolonged, and knock-down of IFIT2 promoted the growth and migra-tion of HepG2 cells.Conclusion FTO may regulate IFIT2 by mediating m6A, and further promote the occurrence and development of HCC.
- Full text:2024073021455588958脂肪量和肥胖相关蛋白FTO...IT2促进肝细胞癌发生发展_兰兰.pdf