Fig. 7

IGF2BP1 rescued the decreased PKM2 stability, repressed glycolysis and inhibited immune escape induced by circFAM13B. A-B QRT-PCR assays showed that the overexpression of IGF2BP1 rescued the attenuation of PKM2 mRNA expression caused by circFAM13B in T24 and UMUC3 cells. (*P < 0.05, **P < 0.01, ***P < 0.001, Student’s t-test). C Western blot assays showed that the overexpression of IGF2BP1 rescued the attenuation of PKM2 protein expression caused by circFAM13B in T24 and UMUC3 cells. D Actinomycin D treatment assays showed that the overexpression of IGF2BP1 rescued the inhibition of mRNA stability caused by circFAM13B in T24 and UMUC3 cells (**P < 0.01, ***P < 0.001, Student’s t-test). E–F Glucose, lactic acid, and ATP detection assays showed that the overexpression of IGF2BP1 rescued the inhibition of glycolysis caused by circFAM13B in T24 and UMUC3 cells (*P < 0.05, **P < 0.01, ***P < 0.001, Student’s t-test). G–H ELISA assays showed that the overexpression of IGF2BP1 weakened the enhancement of granzyme B and IFN-γ production of CD8 + T cells caused by co-culturing with circFAM13B overexpressed T24 and UMUC3 cells (*P < 0.05, **P < 0.01, ***P < 0.001, Student’s t-test). I–J Overexpression of IGF2BP1 weakened the enhanced CD8.⁺ T cells killing ability and increased the immunotherapy sensitivity of BCa cells caused by co-culturing with circFAM13B overexpressed T24 and UMUC3 cells. Data are expressed as mean ± SD, n = 3