RNA-binding protein QKI promotes the progression of HCC by interacting with long non-coding RNA EGOT

• QKI gene expression was increased in tumor tissues and associated with poor prognosis of HCC patients. • QKI protein interacted with EGOT RNA and promoted its expression. • Overexpression of QKI gene promoted the malignancy of HCC cells by promoting EGOT expression in vitro and in vivo . • Overexpression of QKI or EGOT gene activated the SAPK/JNK pathway in HCC cells. RNA-binding proteins are revealed to play important roles during the progression of hepatocellular carcinoma (HCC). However, the regulatory mechanisms of RNA-binding protein Quaking (QKI) in the expression and role of long non-coding RNAs (lncRNAs) in HCC cells remain not well understood. Cell Counting Kit-8, wound-healing, Transwell and colony-forming assays were performed to evaluate the effects of QKI and lncRNA EGOT on proliferation and migration of HCC cells. Tumor growth of HCC was analyzed using a mouse xenograft model. Immunoprecipitation (RIP) assay was used to investigate the interaction between QKI and EGOT. The expression of QKI was significantly upregulated in HCC tissues and the higher QKI level was significantly associated with a poorer prognosis. Overexpression of QKI promoted the proliferation, migration, and colony-forming ability of HCC cells in vitro and tumor growth of HCC in vivo . Mechanistically, QKI protein could bind to EGOT RNA and increase its expression. Inhibition of EGOT attenuated the effects of QKI on the malignant phenotypes of HCC cells. In addition, both QKI and EGOT could activate the SAPK/JNK signaling pathway in HCC cells. Our findings indicated that QKI exerted promotive effects on the malignant phenotypes of HCC through its interaction with EGOT.