Calcium signal modulation in breast cancer aggressiveness

•BC aggressive exhibit high metastatic behavior and early recurrence.•BC aggressive exhibit resistance to therapy and immune escape.•Expression of calcium transporters is altered in the more aggressive BC subtypes.•Calcium remodeling plays a critical role in the BC aggressiveness behavior. Breast ca...

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Bibliographic Details
Published in:Cell calcium (Edinburgh) 2023-07, Vol.113, p.102760-102760, Article 102760
Main Authors: Bantsimba-Malanda, Claudie, Ahidouch, Ahmed, Rodat-Despoix, Lise, Ouadid-Ahidouch, Halima
Format: Article
Language:English
Subjects:
Breast cancer
Breast Neoplasms - metabolism
Calcium
Calcium signaling
Female
Human health and pathology
Humans
Life Sciences
Metastasis
Microenvironment
Poor clinical outcomes
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Summary:•BC aggressive exhibit high metastatic behavior and early recurrence.•BC aggressive exhibit resistance to therapy and immune escape.•Expression of calcium transporters is altered in the more aggressive BC subtypes.•Calcium remodeling plays a critical role in the BC aggressiveness behavior. 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. [Display omitted]
ISSN:0143-4160
1532-1991
DOI:10.1016/j.ceca.2023.102760