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. 2021 Jan 8;40(8):1409–1424. doi: 10.1038/s41388-020-01621-4

Fig. 5. PFKFB3 knockdown enhances the chemosensitivity in EC.

Fig. 5

a, b PFKFB3 was knocked down by CRISPR/Cas9 in HEC-1B and ARK-2 cells. Western blot analysis of PFKFB3 expression was used to examine the effects of PFKFB3-KD in these cells. PCNA was used as a loading control. c, d MTT assays were performed to measure the sensitivity of these cells to chemotherapeutic drugs. Cells were exposed to various doses of carboplatin (CBPt) or cisplatin (Cis) for 48 h after plating. Chemosensitivity represented by IC50 values (e, f) for these cell lines were calculated using GraphPad Prism 7. The data represent as mean ± SD (n = 5, #p < 0.0001). g, h HEC-1B and ARK-2 cells after PFKFB3 knockdown (KD) were treated with or without CBPt (5 μM)/Cis(0.5 μM) for 72 h. Colony formation assay was determined by crystal violet staining. The colony survival rate was calculated using the ImageJ software. The data represent as mean ± SD (n = 3, ***p < 0.001, #p < 0.0001). i, j HEC-1B and ARK-2 cells were treated with or without CBPt (100 μM) for 24 h after PFKFB3 knockdown (KD) and the recognized biomarkers for cell apoptosis, autophagy and Akt/mTOR pathway were determined by Western blot analysis. PCNA was used as the loading control.