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 β-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 β-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.

中文翻译：

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沉默PFKP抑制肝细胞癌细胞的干性

背景

糖酵解重编程与肝细胞癌 (HCC) 的进展密切相关，其中具有干性特征的 HCC 细胞也起着重要作用。因此，糖酵解限速酶磷酸果糖激酶 1 (PFKP) 的血小板同种型是否有助于维持 HCC 细胞的干性，值得研究。

方法

通过蛋白质印迹和免疫组织化学比较人肝细胞癌和邻近正常组织之间的 PFKP 水平。还分析了PFKP表达与临床病理特征的关系。此外，在经历 PFKP 沉默或过表达的 HCC 细胞之间比较了集落形成能力和干细胞标记物（ALDH1、CD44、CD133、Sox-2）以及 β-连环蛋白的水平。

结果

与正常肝组织相比，HCC 中的 PFKP 水平更高。沉默 PFKP 会降低 HCC 增殖、集落形成能力以及干细胞标志物和 β-连环蛋白的水平；而过表达 PFKP 则表现出相反的效果。

结论

PFKP 促进 HCC 增殖并有助于维持 HCC 干性。沉默 PFKP 可以抑制 HCC 的干性，表明 PFKP 可能是 HCC 治疗的潜在治疗靶点。