Extended Data Figure 7: CHD1 shows synthetic essentiality in PTEN-deficient breast cancer.
From: Synthetic essentiality of chromatin remodelling factor CHD1 in PTEN-deficient cancer
a, b, Schematic representations of the role of CHD1 in prostate cancer. In PTEN-intact prostate cells, GSK3β is activated by PTEN through inhibition of AKT and phosphorylates CHD1, which stimulates its degradation through the β-TrCP-mediated ubiquitination–proteasome pathway (a). However, in PTEN-deficient prostate cancer cells, accumulated CHD1 interacts with and maintains H3K4me3, followed by transcriptional activation of genes downstream of NF-κB, leading to disease progression (b). c, Mutual exclusivity of PTEN and CHD1 deletions also occurs in breast cancer and colon cancer. d, e, Immunoblots of lysates and colony-formation assays generated from CHD1-knockdown and control BT549 and MDA-MB-468 cells. f, Growth of subcutaneous tumours derived from CHD1-knockdown MDA-MB-468 cells (control group, n = 10; shCHD1 group, n = 8). Error bars indicate s.d., P values were determined by two-tailed t-test. g, h, Immunoblots of lysates and colony formation assays generated from CHD1-knockdown and control MDA-MB-231 and T47D cells. Representative data of triplicate experiments are shown.
