Fig. 5: The KLF5/Bcl-2/caspase 3 signaling pathway affects the oxaliplatin-induced apoptosis of CRC cells. | Cell Death & Disease

Fig. 5: The KLF5/Bcl-2/caspase 3 signaling pathway affects the oxaliplatin-induced apoptosis of CRC cells.

From: KLF5 inhibition overcomes oxaliplatin resistance in patient-derived colorectal cancer organoids by restoring apoptotic response

Fig. 5

A Western blotting of KLF5, Bcl-2, Bax, cleaved caspase 3 in CRC cell lines. B Knocking down Bcl-2 significantly promoted the expression of cleaved caspase 3, whereas knocking down Bax did not affect the expression of Bcl-2 or cleaved caspase 3 (mean ± SD, n = 3 for each group, Student’s t-test, **P < 0.01, *** p < 0.001). C, D Western blotting showed that inhibiting Bcl-2 can reverse the function of KLF5 in suppressing the expression of cleaved caspase 3, whereas inhibiting Bax cannot reverse the function of KLF5 in cleaved caspase 3 suppression (mean ± SD, n = 3 for each group, one-way ANOVA, **P < 0.01, *** p < 0.001). E KLF5-binding elements (KBE1 to KBE3) on Bcl-2 promoter region. F ChIP verified the direct binding of KLF5 to the predicted site (KBE1) of the Bcl-2 promoter (mean ± SD, n = 3 for each group, Student’s t-test, *** p < 0.001). G The results of luciferase reporter assay showed that KLF5 only promoted the luciferase activity of pGL3-Bcl2-FL (mean ± SD, n = 3 for each group, Student’s t-test, *** p < 0.001). H Schematic diagram showed the mutation site of Bcl-2 Mut 1 and Bcl-2 Mut 2 plasmids. I The results of luciferase reporter assay showed that KLF5 could not promote the luciferase activity of Bcl-2 Mut 1, which did not contain KBE1 sequence (mean ± SD, n = 3 for each group, Student’s t-test, **P < 0.01, *** p < 0.001).

Back to article page