Fig. 5: YAP1/HIF1α contributes to the regulation of HEXB transcription in GBM cells.

a–d qPCR analysis of HEXB mRNA in shHEXB and control GSC1 (a, b) and mGSCs (c, d) under administration of indicated exogenous HEXB recombinant protein (a, c) or Gal-P (b, d), respectively (n = 3 independent samples). e Western blotting analysis of HIF1α and YAP1 protein in Hexb silenced and control mGSCs. (The samples derive from the same experiment but different gels for HEXB, HIF1α, YAP1, P-YAP1, and β-actin were processed in parallel). f Co-IP assays of YAP1 and HIF1α interaction in indicated GSC1 samples. g Western blotting analysis of HIF1α protein stability in GSC1 samples with indicated verteporfin or DMSO treatment (n = 3 independent samples). h Western blotting analysis of HIF1α protein stability in GSC1 transduced with shNC or shHEXB vector, respectively (n = 3 independent samples). i, j Effects of indicated endogenous or exogenous intervention of HEXB on HIF1α transcriptional activity in GSC1(i) and mGSCs (j) (n = 3 independent samples). k qPCR analysis of HEXB mRNA in indicated GSC1 samples with HIF1α overexpression or transfected with YAP-5SA plasmid n = 3 independent samples). l ChIP-PCR assay of GSC1 sample precipitated with HIF1α antibody showing the relative enrichment fold among indicated fragments of HEXB promoters (n = 3 independent samples). m Schematic graphic showing intrinsic regulatory mechanism of HEXB in GBM cells. Data are from 3 (g, right and h, lower) or representative of 3 independent experiments with similar results (a–l). Data were presented as mean ± SEM and analyzed by two-tailed Student’s t-test (a–d,g–l). Source data are provided as a Source Data file.