c-MYC is one of the major proteins that regulate gene expression in cells. c-MYC regulates 2000-3000 genes and accounts for 15% of the entire genome. Therefore, c-MYC is involved in many cellular functions: cell growth, proliferation, differentiation, and apoptosis.
When c-MYC regulation occurs abnormally, it promotes a variety of cancers, such as pancreatic cancer, colon cancer, ovarian cancer, and lymphoma. The c-MYC gene has changed in more than half of human cancers and is often associated with very aggressive tumors.
Researchers at the Spanish National Cancer Research Center (CNIO) have successfully identified a protein that is critical for MYC carcinogenesis in a mouse model. The study used genome-wide data analysis to investigate the behavior of c-MYC in a network of hundreds of genes.
They found c-MYC interacts with BPTF, it is a core subunit of the NURF chromatin-remodelling complex. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. When BPTF is knockdown, c-MYC recruitment to DNA is decreased and chromatin accessibility changes. In Bptf-null MEFs, BPTF is necessary for c-MYC-driven proliferation, G1–S progression and replication stress, but not for c-MYC-driven apoptosis. It is also found that BPTF levels correlate positively with c-MYC-driven transcriptional signatures. In vivo, Bptf inactivation in pre-neoplastic pancreatic acinar cells significantly delays tumour development and extends survival.
This study confirms that blocking BPTF, tumor cells fail to proliferate or their proliferation is inhibited; therefore, the researchers believe that this gene may be a new target for the treatment of many cancer types.
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