Silencing PFKP restrains the stemness of hepatocellular carcinoma cells.

ABSTRACT

BACKGROUND: Glycolysis reprogramming is deeply involved in the progression of hepatocellular carcinoma (HCC), in which HCC cells with stemness traits play important roles as well. Thus, whether platelet isoform of phosphofructokinase 1 (PFKP), a rate-limiting enzyme in glycolysis, contributes to the maintenance of stemness of HCC cells is worth investigation. METHODS: PFKP levels were compared between human hepatocellular carcinoma and adjacent normal tissues by Western blotting and immunohistochemistry. The relationship between PFKP expression and clinic pathological features was also analyzed. Furthermore, the colony formation capabilities and the levels of stemness markers (ALDH1, CD44, CD133, Sox-2) as well as ß-catenin were compared between HCC cells either undergoing PFKP silencing or overexpression. RESULTS: PFKP levels were higher in HCC as compared to normal hepatic tissues. Silencing PFKP decreased HCC proliferation, colony formation capabilities, and levels of stemness markers and ß-catenin; whereas overexpressing PFKP demonstrated the opposite effects. CONCLUSION: PFKP promoted HCC proliferation and contributed to the maintenance of HCC stemness. Silencing PFKP could restrain the stemness of HCC, suggesting that PFKP may be a potential therapeutic target for HCC treatment.