Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
Glycolysis regulator PFKP induces human melanoma cell proliferation and tumor growth.
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Chen Cheng, Zhang Xuejun
Аннотация
PURPOSE: Cutaneous melanoma is an aggressive and deadly cancer resulting from malignant transformation of cells involved in skin pigmentation. Glycolysis is widely implicated in cancer progression, but its precise role in melanoma has not been extensively studied. Here, we investigated the role of the glycolysis regulator phosphofructokinase 1 platelet isoform (PFKP) in melanoma progression.
METHODS: PFKP expression in human melanoma tissues was analyzed by immunohistochemistry. Knockdown of PFKP by siRNA and overexpression of PFKP were performed to evaluate its functions in vitro. CCK-8 assay was used to assess cell proliferation. Glycolytic activity was determined via measurement of extracellular acidification rate (ECAR), lactic acid level, and ATP content. A tumor xenograft model was used to test the function of PFKP in vivo.
RESULTS: PFKP upregulation was observed in human melanoma tissues and correlated with poor patient survival. Knockdown of PFKP in human melanoma cells suppressed cell proliferation and reduced ECAR, ATP levels, and lactic acid levels, while overexpression of PFKP displayed the opposite effects. In vivo, knockdown of PFKP in melanoma cells markedly reduced tumorigenesis. Inhibitory effects on cell proliferation, glycolysis, and tumorigenesis due to PFKP knockdown were further augmented upon treatment with the glycolysis inhibitor 2-deoxy-D-glucose (2-DG).
CONCLUSION: Collectively, these results indicate that PFKP expression in melanoma cells increases proliferation and glycolytic activity in vitro and promotes tumorigenesis in vivo, suggesting that suppression of PKFP and inhibition of glycolysis may potently suppress melanoma progression.
METHODS: PFKP expression in human melanoma tissues was analyzed by immunohistochemistry. Knockdown of PFKP by siRNA and overexpression of PFKP were performed to evaluate its functions in vitro. CCK-8 assay was used to assess cell proliferation. Glycolytic activity was determined via measurement of extracellular acidification rate (ECAR), lactic acid level, and ATP content. A tumor xenograft model was used to test the function of PFKP in vivo.
RESULTS: PFKP upregulation was observed in human melanoma tissues and correlated with poor patient survival. Knockdown of PFKP in human melanoma cells suppressed cell proliferation and reduced ECAR, ATP levels, and lactic acid levels, while overexpression of PFKP displayed the opposite effects. In vivo, knockdown of PFKP in melanoma cells markedly reduced tumorigenesis. Inhibitory effects on cell proliferation, glycolysis, and tumorigenesis due to PFKP knockdown were further augmented upon treatment with the glycolysis inhibitor 2-deoxy-D-glucose (2-DG).
CONCLUSION: Collectively, these results indicate that PFKP expression in melanoma cells increases proliferation and glycolytic activity in vitro and promotes tumorigenesis in vivo, suggesting that suppression of PKFP and inhibition of glycolysis may potently suppress melanoma progression.