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PCK1 attenuates tumor stemness via activating the Hippo signaling pathway in hepatocellular carcinoma

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PCK1 attenuates tumor stemness via activating the Hippo signaling pathway in hepatocellular carcinoma

Liu Rui
Liu Yi
Zhang Wenlu
Zhang Guiji
Zhang Zhirong
Huang Luyi
Tang Ni
Wang Kai
Genes & Diseases第11卷, 第4期纸质出版 2024-07-01在线发表 2023-09-16
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Liver cancer stem cells were found to rely on glycolysis as the preferred metabolic program. Phosphoenolpyruvate carboxylase 1 (PCK1), a gluconeogenic metabolic enzyme, is down-regulated in hepatocellular carcinoma and is closely related to poor prognosis. The oncogenesis and progression of tumors are closely related to cancer stem cells. It is not completely clear whether the PCK1 deficiency increases the stemness of hepatoma cells and promotes the oncogenesis of hepatocellular carcinoma. Herein, the results showed that PCK1 inhibited the self-renewal property of hepatoma cells, reduced the mRNA level of cancer stem cell markers, and inhibited tumorigenesis. Moreover, PCK1 increased the sensitivity of hepatocellular carcinoma cells to sorafenib. Furthermore, we found that PCK1 activated the Hippo pathway by enhancing the phosphorylation of YAP and inhibiting its nuclear translocation. Verteporfin reduced the stemness of hepatoma cells and promoted the pro-apoptotic effect of sorafenib. Thus, combined treatment with verteporfin and sorafenib may be a potential anti-tumor strategy in hepatocellular carcinoma.

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Cancer stem cellsChemoresistanceGluconeogenesisHepatocellular carcinomaYAP