RBMX contributes to hepatocellular carcinoma progression and sorafenib resistance by specifically binding and stabilizing BLACAT1.
Yanan Song, Saifei He, Xing Ma, Miao Zhang, Juhua Zhuang, Guoyu Wang, Ying Ye, Wei Xia
Abstract
database prediction. This mechanism of action is beneficial for cancer cells proliferation, anti-apoptotic, and colony formation with sorafenib treatment. Further, the autophagy level and cancer cell stemness were also improved when RBMX/BLACAT1 upregulated. Our study indicated that hepatoma cells can improve their proliferation, colony ability and autophagy by RBMX stabilizing BLACAT1 expression then promote HCC development and drug resistance. Hence, RBMX could be considered as novel therapeutic target for HCC treatment strategies.
Topics & Concepts
SorafenibCancer researchCarcinogenesisHepatocellular carcinomaAutophagyDownregulation and upregulationCell growthLong non-coding RNARNACancerCancer cellBiologyLiver cancerApoptosisMedicineGeneInternal medicineBiochemistryCancer-related molecular mechanisms researchRNA Research and SplicingRNA modifications and cancer