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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: PDIA3P1 promotes Temozolomide resistance in glioblastoma by inhibiting C/EBPβ degradation to facilitate proneural-to-mesenchymal transition

Fig. 6

PDIA3P1 is upregulated in response to TMZ-induced activation of the p38-MAPK signaling pathway. A B PDIA3P1 expression was induced by TMZ treatment in a dose-dependent (treatment with different concentrations of TMZ for 48 hours) and time-dependent (treatment with 400 μM TMZ for indicated times) manner. C Bubble plot visualized the significantly enriched GO biological pathways using genes upregulated in TMZ-treated GSC group in GSC68029. D Cell viability assay in GSC20, GSC267, U118MG, and U251 treated with different concentrations of NEF for 48 h. E NEF treatment (50 μM, 48 h) abrogated elevation of PDIA3P1 expression induced by TMZ treatment. F Cells were treated with TMZ in combination with NEF at different concentrations and percentages of growth inhibition were visualized. G CI scores of cells treated with TMZ in combination with NEF at different concentrations. H Pearson correlation test was performed to show the correlation of PDIA3P1 expression with JUN in TCGA and CGGA datasets, respectively. I Knocking down of JUN expression using siRNA reduced the expression of PDIA3P1 (left panel). Knocking down of JUN counteracted TMZ treatment (400 μM, 48 h) induced upregulation of PDIA3P1 (right panel). J The recognition motif of JUN obtained from the JASPAR (upper panel) and schematic illustration of four fragments in promoter sequence of PDIA3P1 (lower panel). K The luciferase assay showed PDIA3P1 knockdown reduced promoter activity in fragments 1–3. L ChIP-PCR assay showed that JUN bound to a predicted site within the PDIA3P1 promoter

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