4. Conclusion:
We report herein that 5,6-ECs are at the center of a newly discovered metabolic branch that controls carcinogenesis (Fig 4). The identification of oncosterone, its biosynthetic pathway and its effectors, highlights the existence of interesting targets for the development of anticancer drugs applicable for TNBC treatment (Fig 5). This is reminiscent of the development of targeted therapeutic strategies against the tumour promoter 17β-oestradiol for ER(+)-BC treatment (Simpson & Santen, 2015). On the other hand, studies of the 5,6α-EC metabolism in normal tissues led to the identification of DDA. Surprisingly DDA was found to display tumour suppressor properties on BC through the activation of cell differentiation and death programs, and the inhibition of oncosterone biosynthesis, highlighting the existence of a metabolic balance between the tumour promoteur oncosterone and the tumour suppressor DDA. This opens up new options for the development of new anticancer agents targeting the oncosterone pathway in BC and new strategies for the chemoprevention of BC. This also provides a new rational at the molecular level to study potential relationships that may exist between cholesterol, diet and BC oncogenesis programs (Silvente-Poirot, Dalenc & Poirot, 2018).