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. 2023 Oct 23;51(21):11634–11651. doi: 10.1093/nar/gkad907

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© The Author(s) 2023. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 6. — BRD9 contributes to the development of cancer cells via regulating the TGF-β pathway. (A) Transcript levels of BRD9 in non-tumor tissue and pancreatic adenocarcinoma (PAAD) samples (GSE28735). (B) BRD9 protein levels in normal tissue and stage 1, 2, 3 and 4 PAAD samples in the Clinical Proteomic Tumor Analysis Consortium (CPTAC) dataset. (C) Inhibition of BRD9 with I-BRD9 reduces BxPC3 cell proliferation. The cell number was measured from day 0 to day 3 after 10 μM I-BRD9 treatment. (D) The effect of BRD9 inhibition on BxPC3 cell vitality. MTT assays were performed to measure cell vitality (OD 570 nm, n = 5). (E) I-BRD9 impairs colony formation ability of BxPC3 cells. The colony formation assay of BxPC3 with or without 10 days of I-BRD9 treatment (10 μM) was performed. (F) I-BRD9 reduces the migration ability of pancreatic cancer cells. Wound healing experiments were performed with I-BRD9 (10 μM) or DMSO treatment in the BxPC3 cell line. (G) KEGG analysis of differentially expressed genes (DEGs) in PAAD from the GSE28735 dataset. (H) Inhibition of TGF-β signaling reduces proliferation of pancreatic cancer cells. Cell numbers were measured after I-BRD9 (10 μM), SB431542 (10 μM) or SIS3 (10 μM) treatment in the BxPC3 cell line. (I) Inhibition of BRD9 reduces the expression of TGF-β signaling-associated genes in BxPC3 cells. The expression of TGF-β signaling-associated genes was measured after treatment with 10 μM I-BRD9 for 48 h. (J) Overexpression of BRD9 prompts the expression of TGF-β signaling-associated genes in pancreatic cancer cells. The expression of TGF-β signaling-associated genes was measured in control and BRD9-overexpressing BxPC3 cells. (K) Western blot for SMAD2 and p-SMAD2 protein levels in BxPC3 cells upon BRD9 inhibition with 10 μM I-BRD9 for 48 h. (L) qPCR analysis shows reduced expression of WNT3 and WNT3A genes in BxPC3 cells upon treatment with 10 μM I-BRD9 for 48 h. (M) Viability of BxPC3 cells after treatment with IWR-1, IWP-2 or DKK1. Viability was measured using the MTT assay and no significant changes were observed with 1 μM IWR-1, 5 μM IWP-2 or 10 ng/ml DKK1 treatment. (N) Inhibition of BRD9 reduces expression of TGF-β signaling-associated genes in MCF7 cells. The expression of TGF-β signaling-associated genes was measured after treatment with 10 μM I-BRD9 for 2 days. (O) Treatment with the BRD9 inhibitor I-BRD9 or the TGF-β signaling pathway inhibitor SB431542 reduces MCF7 cell proliferation. Cell numbers were measured from day 0 to day 3 after treatment with indicated inhibitors. (P) Treatment of BxPC3 cells with gemcitabine (GEM) increases expression of TGF-β signaling-associated genes. The expression of TGF-β signaling-associated genes was measured after treatment with 20 μM GEM for 2 days. (Q) Treatment of BxPC3 cells with GEM, I-BRD9 or both reduces cell proliferation. Cell numbers were measured after 48 h of treatment with 20 μM GEM, 10 or 20 μM I-BRD9 or a combination of both.