Expression of plasma membrane calcium pump isoform mRNAs in breast cancer cell lines

Lee, Won Jae; Roberts‐Thomson, Sarah J.; Holman, N. A.; May, Fiona J.; Lehrbach, Gillian M.; Monteith, Gregory R.

doi:10.1016/s0898-6568(02)00049-9

Cited by 57 publications

(46 citation statements)

References 32 publications

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“…The essential roles of the SOCC Orai1 and the signaling molecule Stim1 in breast cancer metastasis formation was recently reported (31). Monteith and his group (12) observed that the expression of different isoforms of the PMCA is changed in breast cancer cells and that PMCA2 expression is significantly increased (32). Furthermore, inhibition of PMCA using siRNA decreased proliferation of MCF-7 human breast cancer cells (33).…”

Section: Discussionmentioning

confidence: 99%

Tamoxifen Inhibits TRPV6 Activity via Estrogen Receptor–Independent Pathways in TRPV6-Expressing MCF-7 Breast Cancer Cells

Bolanz

Kovács

Landowski

et al. 2009

Molecular Cancer Research

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The epithelial calcium channel TRPV6 is upregulated in breast carcinoma compared with normal mammary gland tissue. The selective estrogen receptor modulator tamoxifen is widely used in breast cancer therapy. Previously, we showed that tamoxifen inhibits calcium uptake in TRPV6-transfected Xenopus oocytes. In this study, we examined the effect of tamoxifen on TRPV6 function and intracellular calcium homeostasis in MCF-7 breast cancer cells transiently transfected with EYFP-C1-TRPV6. TRPV6 activity was measured with fluorescence microscopy using Fura-2. The basal calcium level was higher in transfected cells compared with nontransfected cells in calcium-containing solution but not in nominally calcium-free buffer. Basal influxes of calcium and barium were also increased. In transfected cells, 10 μmol/L tamoxifen reduced the basal intracellular calcium concentration to the basal calcium level of nontransfected cells. Tamoxifen decreased the transport rates of calcium and barium in transfected cells by 50%. This inhibitory effect was not blocked by the estrogen receptor antagonist, ICI 182,720. Similarly, a tamoxifen-induced inhibitory effect was also observed in MDA-MB-231 estrogen receptor-negative cells. The effect of tamoxifen was completely blocked by activation of protein kinase C. Inhibiting protein kinase C with calphostin C decreased TRPV6 activity but did not alter the effect of tamoxifen. These findings illustrate how tamoxifen might be effective in estrogen receptor-negative breast carcinomas and suggest that the therapeutic effect of tamoxifen and protein kinase C inhibitors used in breast cancer therapy might involve TRPV6-mediated calcium entry. This study highlights a possible role of TRPV6 as therapeutic target in breast cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Tamoxifen Inhibits TRPV6 Activity via Estrogen Receptor–Independent Pathways in TRPV6-Expressing MCF-7 Breast Cancer Cells

Bolanz

Kovács

Landowski

et al. 2009

Molecular Cancer Research

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“…A recent study showed that elevated PMCA2 expression in mammary epithelial cells inhibited apoptosis and in human breast cancer cases a high PMCA2 mRNA level was associated with poor clinical prognosis [62]. In breast cancer cell lines PMCA1 and PMCA2 was shown to be expressed at an increased level compared to non-tumorigenic cells [11,12] although, in one study PMCA2 mRNA was not detected by RT-PCR in MCF-7 cells [63]. By real-time quantitative PCR we also observed the expression of all three PMCA isoforms (PMCA1, 2 and 4), however, at the protein level, we found only PMCA1 with some PMCA4 expression in MCF-7 cells.…”

Section: Discussionmentioning

confidence: 99%

“…mRNA expression studies on breast cancer cell lines showed upreguleted PMCA1 and 2 and downregulated PMCA4 expression in some breast cancer cells compared to non-tumorigenic cell lines [11,12]. PMCA1 was found to be epigenetically inactivated in oral squamous cell carcinoma-derived cell lines, and PMCA1 protein was frequently downregulated in primary oral squamous cell carcinoma and oral premalignant lesion tissue samples [13].…”

Section: Introductionmentioning

confidence: 99%

Histone deacetylase inhibitor- and PMA-induced upregulation of PMCA4b enhances Ca2+ clearance from MCF-7 breast cancer cells

et al. 2014

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The expression of the plasma membrane Ca 2+ ATPase (PMCA) isoforms is altered in several types of cancer cells suggesting that they are involved in cancer progression. In this study we induced differentiation of MCF-7 breast cancer cells by histone deacetylase inhibitors (HDACis) such as short chain fatty acids (SCFAs) or suberoylanilide hydroxamic acid (SAHA), and by phorbol 12-myristate 13-acetate (PMA) and found strong upregulation of PMCA4b protein expression in response to these treatments. Furthermore, combination of HDACis with PMA augmented cell differentiation and further enhanced PMCA4b expression both at mRNA and protein levels. Immunocytochemical analysis revealed that the upregulated protein was located mostly in the plasma membrane. To examine the functional consequences of elevated PMCA4b expression, the characteristics of intracellular Ca 2+ signals were investigated before and after differentiation inducing treatments, and also in cells overexpressing PMCA4b. The increased PMCA4b expression -either by treatment or overexpression -led to enhanced Ca 2+ clearance from the stimulated cells. We found pronounced PMCA4 protein expression in normal breast tissue samples highlighting the importance of this pump for the maintenance of mammary epithelial Ca 2+ homeostasis. These results suggest that modulation of Ca 2+ signaling by enhanced PMCA4b expression may contribute to normal development of breast epithelium and may be lost in cancer.3

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“…Indeed, relative PMCA1 mRNA expression is greater in tumorigenic breast cancer MCF-7 and MDA-MB-231 cells than that in non-tumorigenic MCF-10A cells (21). PMCA1 and PMCA4 expression is also lower in simian virus 40-transformed human skin fibroblasts (22).…”

Section: Free Intracellular Camentioning

confidence: 97%

Antisense-mediated Inhibition of the Plasma Membrane Calcium-ATPase Suppresses Proliferation of MCF-7 Cells

Lee

Robinson

Holman

et al. 2005

Journal of Biological Chemistry

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Alterations in Ca2؉ signaling may contribute to tumorigenesis and the mechanism of action of some anticancer drugs. The plasma membrane calcium-ATPase (PMCA) is a crucial controller of intracellular Ca 2؉ signaling. Altered PMCA expression occurs in the mammary gland during lactation and in breast cancer cell lines. Despite this, the consequences of PMCA inhibition in breast cancer cell lines have not been investigated. In this work, we used Tet-off PMCA antisense-expressing MCF-7 cells to assess the effects of PMCA inhibition in a human breast cancer cell line. At a level of PMCA inhibition that did not completely prevent PMCA-mediated Ca 2؉ efflux and did not induce cell death, a dramatic inhibition of cellular proliferation was observed. Fluorescence-activated cell sorting analysis indicated that PMCA antisense involves changes in cell cycle kinetics but not cell cycle arrest. We concluded that modulation of PMCA has important effects in regulating the proliferation of human breast cancer MCF-7 cells.

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Expression of plasma membrane calcium pump isoform mRNAs in breast cancer cell lines

Cited by 57 publications

References 32 publications

Tamoxifen Inhibits TRPV6 Activity via Estrogen Receptor–Independent Pathways in TRPV6-Expressing MCF-7 Breast Cancer Cells

Tamoxifen Inhibits TRPV6 Activity via Estrogen Receptor–Independent Pathways in TRPV6-Expressing MCF-7 Breast Cancer Cells

Histone deacetylase inhibitor- and PMA-induced upregulation of PMCA4b enhances Ca2+ clearance from MCF-7 breast cancer cells

Antisense-mediated Inhibition of the Plasma Membrane Calcium-ATPase Suppresses Proliferation of MCF-7 Cells

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