GSE211804
FIT Links c-Myc and P53 Acetylation by Recruiting RBBP7 During Carcinogenesis of Colorectal Cancer
Colorectal cancer (CRC) poses one of the most serious threat against human health worldwide, and abnormally expressed c-Myc and p53 are deemed the pivotal driving forces of CRC progression. Here we discovered a lncRNA FIT, which was down-regulated in CRC clinical samples, was transcriptionally suppressed by c-Myc and promoted CRC cells apoptosis by inducing FAS expression. FAS is a p53 target gene, and we found that FIT formed a trimer with RBBP7 and p53 which facilitated p53 acetylation and transcription. Moreover, FIT was capable of retarding CRC growth in mice xenograft model and positively relevant to FAS expression clinically. Thereby our study elucidated the role of lncRNA FIT in human colorectal cancer growth and provides a potential target for anti-CRC drugs. Overall design: lncRNA and mRNA expression for CRC tissue ,pCDH and pCDH-lnc-FIT in HCT116 cells by high throughput sequencing