Abstract:
:Over 70% of human breast cancers are estrogen receptor-positive (ER+), most of which express MYB. In these and other cell types, the MYB transcription factor regulates the expression of many genes involved in cell proliferation, differentiation, tumorigenesis, and apoptosis. So far, no clear link has been established between MYB and the DNA damage response in breast cancer. Here, we found that silencing MYB in the ER+ breast cancer cell line MCF-7 led to increased DNA damage accumulation, as marked by increased γ-H2AX foci following induction of double-stranded breaks. We further found that this was likely mediated by decreased homologous recombination-mediated repair (HRR), since silencing MYB impaired the formation of RAD51 foci in response to DNA damage. Moreover, cells depleted for MYB exhibited reduced expression of several key genes involved in HRR including BRCA1, PALB2, and TOPBP1. Taken together, these data imply that MYB and its targets play an important role in the response of ER+ breast cancer cells to DNA damage, and suggest that induction of DNA damage along with inhibition of MYB activity could offer therapeutic benefits for ER+ breast cancer and possibly other cancer types.
journal_name
Oncogenejournal_title
Oncogeneauthors
Yang RM,Nanayakkara D,Kalimutho M,Mitra P,Khanna KK,Dray E,Gonda TJdoi
10.1038/s41388-019-0789-3subject
Has Abstractpub_date
2019-06-01 00:00:00pages
5239-5249issue
26eissn
0950-9232issn
1476-5594pii
10.1038/s41388-019-0789-3journal_volume
38pub_type
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