Abstract
Breast cancer (BC) is the second most common cancer and cause of death in women. The aggressive subtypes including triple negative types (TNBCs) show a resistance to chemotherapy, impaired immune system, and a worse prognosis. From a histological point of view, TNBCs are deficient in oestrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2+) expression. Many studies reported an alteration in the expression of calcium channels, calcium binding proteins and pumps in BC that promote proliferation, survival, resistance to chemotherapy, and metastasis. Moreover, Ca2+ signal remodeling and calcium transporters expression have been associated to TNBCs and HER2+ BC subtypes.This review provides insight into the underlying alteration of the expression of calcium-permeable channels, pumps, and calcium dependent proteins and how this alteration plays an important role in promoting metastasis, metabolic switching, inflammation, and escape to chemotherapy treatment and immune surveillance in aggressive BC including TNBCs models and highly metastatic BC tumors.
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