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Background  Remodeling of Ca 2+  signaling is an important step in cancer progression, and altered expression of members of the Ca 2+  signaling toolkit including the plasma membrane Ca 2+  ATPases (PMCA proteins encoded by  ATP2B  genes) is common in tumors.    Methods  In this study PMCAs were examined in breast cancer datasets and in a variety of breast cancer cell lines representing different subtypes. We investigated how estrogen receptor alpha (ER-α) and histone deacetylase (HDAC) inhibitors regulate the expression of these pumps.    Results  Three distinct datasets displayed significantly lower  ATP2B4  mRNA expression in invasive breast cancer tissue samples compared to normal breast tissue, whereas the expression of  ATP2B1  and  ATP2B2  was not altered. Studying the protein expression profiles of Ca 2+  pumps in a variety of breast cancer cell lines revealed low PMCA4b expression in the ER-α positive cells, and its marked upregulation upon HDAC inhibitor treatments. PMCA4b expression was also positively regulated by the ER-α pathway in MCF-7 cells that led to enhanced Ca 2+  extrusion capacity in response to 17β-estradiol (E2) treatment. E2-induced PMCA4b expression was further augmented by HDAC inhibitors. Surprisingly, E2 did not affect the expression of PMCA4b in other ER-α positive cells ZR-75-1, T-47D and BT-474. These findings were in good accordance with ChIP-seq data analysis that revealed an ER-α binding site in the  ATP2B4  gene in MCF-7 cells but not in other ER-α positive tumor cells. In the triple negative cells PMCA4b expression was relatively high, and the effect of HDAC inhibitor treatment was less pronounced as compared to that of the ER-α positive cells. Although, the expression of PMCA4b was relatively high in the triple negative cells, a fraction of the protein was found in intracellular compartments that could interfere with the cellular function of the protein.    Conclusions  Our results suggest that the expression of Ca 2+  pumps is highly regulated in breast cancer cells in a subtype specific manner. Our results suggest that hormonal imbalances, epigenetic modifications and impaired protein trafficking could interfere with the expression and cellular function of PMCA4b in the course of breast cancer progression.    Electronic supplementary material  The online version of this article (10.1186/s12885-018-4945-x) contains supplementary material, which is available to authorized users.

Expression of calcium pumps is differentially regulated by histone deacetylase inhibitors and estrogen receptor alpha in breast cancer cells