Skip to main content
. 2021 May 15;41(7):560–575. doi: 10.1002/cac2.12158

FIGURE 1.

FIGURE 1

PKM2 promotes glucose metabolism in bladder cancer cells and predicts poor survival in BCa patients. (A) PKM2 is higher in BCa tissues than in normal tissues (TCGA database). (B) The OS curves show that PKM2 predicts poor prognosis for BCa (TCGA database). (C) PKM2 mRNA is up‐regulated in BCa tissues as compared with adjacent normal tissues by qRT‐PCR. (D) Kaplan‐Meier survival curves show that PKM2 up‐regulation is significantly associated with poor OS and RFS in BCa patients. (E) Validation of the overexpression efficacy of PKM2 in 5637 and T24 cell lines by Western blotting. (F,G,H) Effects of PKM2 overexpression on glucose utilization, lactic acid production, and intracellular ATP production measured by glucose assay, lactic acid assay, and intracellular ATP assay in 5637 and T24 cells. (I) PKM2 contributes to the proliferation of 5637 and T24 cells as measured by CCK‐8 assays. (J) PKM2 contributes to the colony formation of 5637 and T24 cells as measured by colony formation assays. * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: PKM2, pyruvate kinase muscle isozyme M2; GFP, green fluorescent protein; BCa, bladder cancer; TCGA, The Cancer Genome Atlas; OS, overall survival; qRT‐PCR, quantitative real‐time polymerase chain reaction; RFS, recurrence‐free survival; ATP: adenosine triphosphate; FPKM, fragments per kilobase million values; CCK‐8, cell counting kit‐8.