Fig. 3: BR0063 inhibits proliferation in DMS 114 and MFE-296 cells by p16-induced cell senescence. | Cell Death & Disease

Fig. 3: BR0063 inhibits proliferation in DMS 114 and MFE-296 cells by p16-induced cell senescence.

From: Hypermethylation of CDKN2A CpG island drives resistance to PRC2 inhibitors in SWI/SNF loss-of-function tumors

Fig. 3

A Flow cytometry analysis for cell cycle distribution of control and BR0063-treated DMS 114 and MFE-296 cells by PI staining. The result of one representative assay from two similar independent experiments is shown, with x- and y axes denote PI signal and cell number count, respectively. Only intact and single cells are included in the analysis. Cell population fitted in G1 phase are marked as blue, S phase as yellow, G2/M phase as green. The distribution of the sum of the fitted cell population shown as magenta overlaps with the original distribution shown as black. B β-galactosidase staining of DMSO- or BR0063-treated DMS 114 and MFE-296 cells (at ×200 magnification). C Caspase-3/7 assay detection of apoptosis in control and BR0063-treated DMS 114 and MFE-296 cells, with the addition of positive control, oxaliplatin, which is known to induce cellular apoptosis. Each experiment was performed in triplicate, and error bars are shown as the mean ± SD. D CellTiter-Glo® detection of cell viability of DMS 114 (with or without Dox-induced p16 knockdown) incubated with serial dilution of BR0063 for 14 days, normalized with DMSO control. Each experiment was performed in triplicate, and error bars are shown as the mean ± SD. E, F WB and qPCR analyses of DMS 114 cells treated with control or BR0063, with or without Dox-induced p16 knockdown. For the qPCR analyses, each sample was run in triplicate, and error bars represent the mean ± SD.

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