Two existing cancer drugs turn on a gene that tells tumor cells to remain inactive, according to a study led by researchers at the Icahn School of Medicine at Mount Sinai and published today in Nature Communications.
Researchers discovered that the gene NR2F1, when switched on, programs tumor cells to stay dormant. When the gene is switched off, tumor cells divide and multiply as part of abnormal growth, potentially allowing dormant cells to grow into tumors throughout the body (metastasis). Combining the anticancer drugs azacytidine and retinoic acid significantly increased the amount of active NR2F1 in tumor cells. These patterns were found in mouse models of several cancers, and confirmed in prostate cancer cells from human patients.
Results suggest that NR2F1 is a “master regulator” of tumor cell growth, influencing several genes that determine whether cells remain inactive, or quiescent in medical terms. According to the study, NR2F1 exerts…
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