Professor Xianghui Fu and his research team of the State Key Laboratory of Biotherapy, West China Hospital has recently published an articled “MITA1, an Energy Stress–Inducible Long Noncoding RNA, Promotes Hepatocellular Carcinoma Metastasis” in Hepatology ( JIF: 14.079 ). This article has identified the funuction and mechanism of a novel lncRNA, termed metabolism--induced tumor activator 1 ( MITA1 ), in hepatocellular carcinoma ( HCC ) and its metastasis. The State Key Laboratory of Biotherapy, West China Hospital is the first author and the corresponding work unit; and Professor Xianghui Fu and Associate Professor Yan Tian are the corresponding authors.
Nutrition deficiency is an important feature of solid tumor microenvironment, but its role in the growth and metastasis of tumor cells and its regulatory mechanism remain unclear. Professor Fu’s team identified a number of long non-coding RNA ( lncRNA ) regulated by energy stress using a unique high-throughput sequencing method of nuclear RNA, and expounded the function and mechanism of the new lncRNA MITA1 ( Metabolism-induced tumor activitor 1 ) in hepatocellular carcinoma. This study found that under nutritional deficiency, energy metabolic receptor "AMPK" activates and promotes the binding of DNA methylase DNMT3B and acts as CpG island of MITA1 intron, which improves its DNA methylation level, and then up-regulates the expression of MITA1. “Correspondingly, there is a positive correlation between the levels of MITA1 and Slug precursors in HCC tissues. Conclusion: Our data reveal MITA1 as a crucial driver of HCC metastasis, and highlight the newly identified AMPK‐MITA1‐Slug axis as a potential therapeutic strategy for HCC.”
The research has received financial support from the Major New Drug Creation Project of the Ministry of Science and Technology of the People’s Republic of China, the Major Research Program, General Program and Youth Project of the National Natural Science Foundation of China.
Full Article Link: https://aasldpubs.onlinelibrary.wiley.com/doi/abs/10.1002/hep.30602
