Project description:The incidence of TP53 loss-of-function in hepatocellular carcinoma is very high. In order to clarify the gene expression differences induced by the changes of TP53 gene, we used two human hepatocellular carcinoma cell lines, SK-HEP-1 and Hep 3B with TP53 knockdown or overexpression for RNA sequencing . SK-HEP-1 is a TP53 wild-type hepatocellular carcinoma cell line. Thus, we knockdown TP53 in SK-HEP-1. Hep 3B is a TP53 loss-of-function hepatocellular carcinoma cell line. Thus, we overexpress TP53 in Hep 3B. Results of RNA-seq analysis showed the differences after knocking-down or overexpressing TP53.
Project description:In this study, we demonstrated that mitochondrial respiratory defect enhanced NFE2L1 transcription via reactive oxygen species (ROS)-mediated STAT3 activation and the up-expressed NFE2L1 increased hepatoma cell invasiveness by inducing syntaxin 12 (STX12) expression. Bioinformatic analysis of The Cancer Genome Atlas Liver Hepatocellular carcinoma (TCGA-LIHC) open database showed that NFE2L1 expression is strongly positively correlated with STX12 expression and, furthermore, epithelial-mesenchymal transition (EMT)-related core genes were significantly upregulated in the tumors expressing both NFE2L1 and STX12. The effect of NFE2L1/STX12 axis on lung metastasis of hepatoma cell was proved in nude mice model. Collectively, our results indicate that NFE2L1 was a key mitochondrial retrograde signaling-mediated primary gene product to enhance hepatoma cell invasiveness via STX12 expression