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The circadian clock confers daily rhythmicity on many biochemical and physiological functions and its disruption is associated with increased risks of developing obesity, diabetes, heart disease and cancer. Although, there are studies on the role of  Bmal1  in carcinogenesis using germline, conditional or tissue-specific knockouts, it is still not well understood how  BMAL1  gene affects cancer-related biological events at the molecular level. We, therefore, took an  in vitro  approach to understand the contribution of  BMAL1  in this molecular mechanism using human breast epithelial cell lines by knocking out  BMAL1  gene with CRISPR technology. We preferred epithelial cells over fibroblasts as the most of cancers originate from epithelial cells. After obtaining  BMAL1  knockouts by targeting the gene at two different sites from non-tumorigenic MCF10A and invasive tumorigenic MDA-MB-231 cells, we analysed apoptosis and invasion properties of the cell lines as representative events in tumor development.  BMAL1  disruption sensitized both cell lines to a bulky-DNA adduct forming agent (cisplatin) and a double-strand break-inducing agent (doxorubicin), while it enhanced the invasive properties of MDA-MB-231 cells. These results show that the disruption of clock genes may have opposing carcinogenic effects.

Opposite Carcinogenic Effects of Circadian Clock Gene BMAL1