tailieunhanh - Overexpression of PFKFB3 promotes cell glycolysis and proliferation in renal cell carcinoma

Cancer cells prefer utilizing aerobic glycolysis in order to exacerbate tumor mass and maintain un-regulated proliferative rates. As a key glycolytic activator, phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) has been implicated in multiple tumor type progression. | Li et al. BMC Cancer 2022 22 83 https s12885-022-09183-2 RESEARCH Open Access Overexpression of PFKFB3 promotes cell glycolysis and proliferation in renal cell carcinoma Jun Li1 Shiqiang Zhang1 Dingzhun Liao2 Qian Zhang3 Chujie Chen1 Xiangwei Yang1 Donggen Jiang1 and Jun Pang1 Abstract Background Cancer cells prefer utilizing aerobic glycolysis in order to exacerbate tumor mass and maintain un-reg- ulated proliferative rates. As a key glycolytic activator phosphofructo-2-kinase fructose-2 6-bisphosphatase 3 PFKFB3 has been implicated in multiple tumor type progression. However the specific function and clinical significance of PFKFB3 in renal cell carcinoma RCC are yet not clarified. This investigation assessed PFKFB3 roles in RCC. Methods PFKFB3 expression levels were analyzed in clear cell renal cell carcinoma ccRCC tissues together with its relationship with clinical characteristics of ccRCC. Real-time PCR and Western blot assays were employed for deter- mining PFKFB3 expression in different RCC cell lines. Furthermore we determined the glycolytic activity by glucose uptake lactate secretion assay and ECAR analysis. CCK-8 assay clone formation flow cytometry and EdU assessments were performed for monitoring tumor proliferative capacity and cell-cycle distribution. Furthermore a murine xeno- graft model was employed for investigating the effect of PFKFB3 on tumor growth in vivo. Results PFKFB3 was significantly up-regulated in RCC specimens and cell lines in comparison to normal control. Overexpression of PFKFB3 was directly correlated to later TNM stages thus becoming a robust prognostic biomarker for ccRCC cases. Furthermore PFKFB3 knockdown suppressed cell glycolysis proliferative rate and cell-cycle G1 S conversion in RCC cells. Importantly in vivo experiments confirmed that PFKFB3 knockdown delayed tumor growth derived from the ACHN cell line. Conclusions Such results suggest that PFKFB3 is a key molecular player in RCC progression via .