**3.2. Voltage-gated calcium channels as pharmacological targets in breast cancer**

1 mM Mn2+ and 0.1 mM Ni2+ ions blocked the fast activation and inactivation of the T-type calcium currents in MCF7 breast cancer cells [79].

Low doses (10–20 μM) of verapamil, an antagonist of voltage-gated calcium channels, blocked the growth of triple-negative MDA-MB-231 breast cancer cells, while high doses (100 μM) reduced by 90% the triple-negative MDA-MB-231 and MCF7 breast cancer cells [76].

Cav3.2 channels were demonstrated to play an important role in the mechanisms involved in chemoresistance. To date, trastuzumab resistance was demonstrated to be correlated with high mRNA Cav3.2 levels in SKBR3 breast cancer cells [120]. Patients with estrogen receptor-positive breast cancer that had a poor clinical outcome presented a significant Cav3.2 upregulation [120]. Moreover, patients with HER2-positive breast cancer presented a positive correlation between the Cav3.2 expression and patient survival upon chemotherapy [120].
