Fig. 5: TRIM25 activates YB1/Bcl-2 transcription axis through ubiquitin proteasome pathway-mediated degradation of BRD7 protein in breast cancer cells. | Cell Death & Disease

Fig. 5: TRIM25 activates YB1/Bcl-2 transcription axis through ubiquitin proteasome pathway-mediated degradation of BRD7 protein in breast cancer cells.

From: TRIM25 degrades BRD7 protein stability through the ubiquitin proteasome pathway to promote breast cancer progression and paclitaxel resistance by activating YB1/Bcl-2 transcription axis

Fig. 5: TRIM25 activates YB1/Bcl-2 transcription axis through ubiquitin proteasome pathway-mediated degradation of BRD7 protein in breast cancer cells.

A MDA-MB-231 and MCF7 cells were transfected with vector or TRIM25 plasmids, the expression level of BRD7 and YB1 were detected by western blot. B BC cells were transfected with siNC, siTRIM25#1 or siTRIM25#2, the expression of BRD7 and YB1 were detected by western blot. C RT-qPCR analysis was performed to analyze the mRNA expression level of Bcl-2 in YB1 overexpression and knockdown BC cells. D Bcl-2 expression was detected by western blot assay under YB1 overexpression. E Bcl-2 expression was detected by western blot assay after YB1 knockdown. F ChIP-qPCR was used to analyze the enrichment region of YB1 on Bcl-2 promoter fragments. G Bcl-2 expression was detected by western blot after BRD7 overexpression or restoring YB1 expression. H Western blot was used to detect the alterations of expression of YB1 and Bcl-2 after TRIM25 knockdown or BRD7 restoration. Data are shown as the mean ± SD of at least three independent experiments, and the significant level was identified by **P < 0.01 and ***P < 0.001.

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