Article | 16 September 2020

This manuscript provides a simplified overview of the involvement of mitochondrial activity and OXPHOS in the metastasis of breast cancer with calcification. We propose that massive accumulation of calcified granules due to breast cancer necrosis or deposition of spontaneous secretions around the glands lead to reprogramming of tumour metabolism, particularly enhancement of mitochondrial metabolism. Upregulation of the OXPHOS complex and subsequent activation of TGFβ-SMAD and MAPK (e.g., JNK, ERK, P38) signalling pathways facilitate the EMT process of breast cancer cells. Interestingly, the OXPHOS inhibitor rotenone could block the EMT process due to cell calcification.