Regulation of Ca2+ mobilization by prolactin in mammary gland cells: Possible role of secretory pathway Ca2+-ATPase type 2

Anantamongkol, Utchariya; Takemura, Hiroyuki; Suthiphongchai, Tuangporn; Krishnamra, Nateetip; Horio, Yoshiyuki

doi:10.1016/j.bbrc.2006.11.055

Cited by 23 publications

(21 citation statements)

References 19 publications

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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%

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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Section: Discussionmentioning

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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“…Indeed, the overall expression pattern for Atp2c2 correlated predominantly with MIST1 expression. Previous studies have revealed that Atp2c2 is expressed in a number of tissues, most notably in the testes, brain and lactating mammary gland [20, 21]. While MIST1 is not found in testes or brain, it is expressed transiently in epithelial alveolar cells during lactation [20].…”

Section: Discussionmentioning

confidence: 99%

MIST1 regulates the pancreatic acinar cell expression of Atp2c2, the gene encoding secretory pathway calcium ATPase 2

Garside¹,

Kowalik²,

Johnson³

et al. 2010

Experimental Cell Research

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MIST1 is a transcription factor expressed in pancreatic acinar cells and other serous exocrine cells. Mice harboring a targeted deletion of the Mist1 gene (Mist1−/−) exhibit alterations in acinar regulated exocytosis and aberrant Ca2+ signaling that are normally controlled by acinar cell Ca2+-ATPases. Previous studies indicated that total sarcoendoplasmic reticulum Ca2+-ATPases (SERCA) and plasma membrane Ca2+-ATPases (PMCA) remained unaffected in Mist1−/− acinar cultures. Therefore, we have assessed the expression of Atp2c2, the gene that encodes the secretory pathway Ca2+-ATPase 2 (SPCA2). We revealed a dramatic decrease in pancreatic expression of Atp2a2 mRNA and SPCA2 protein in Mist1−/− mice. Surprisingly, this analysis indicated that the acinar-specific Atp2c2 mRNA is a novel transcript, consisting of only the 3′ end of the gene and the protein and localizes to the endoplasmic reticulum. Expression of SPCA2 was also lost in Mist1−/− secretory cells of the salivary glands and seminal vesicles, suggesting that Atp2c2 transcription is regulated by MIST1. Indeed, inducible MIST1 expression in Mist1−/− pancreatic acinar cells restored normal Atp2c2 expression, supporting a role for MIST1 in regulating the Atp2c2 gene. Based on these results, we have identified a new Atp2c2 transcript, the loss of which may be linked to the Mist1−/− phenotype.

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“…4B in set), and the b/a ratio was calculated for the different concentrations (0.5-10 µM). Figure 4B shows that under control conditions (i.e., exposure to ATP alone) Thapsigargin, an inhibitor of the SERCA, allows Ca 2+ to leak out from the ER pool [19] causing complete store depletion also in MCF-7 cells [29]. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 13 acac)(DMS)] on Ca 2+ influx using buffers with Na + concentrations being 0 and 140 mM.…”

Section: + -Atpases Activitymentioning

confidence: 99%

The platinum (II) complex [Pt(O,O′-acac)(γ-acac)(DMS)] alters the intracellular calcium homeostasis in MCF-7 breast cancer cells

Muscella

Calabriso

Vetrugno

et al. 2011

Biochemical Pharmacology

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Regulation of Ca2+ mobilization by prolactin in mammary gland cells: Possible role of secretory pathway Ca2+-ATPase type 2

Cited by 23 publications

References 19 publications

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

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

MIST1 regulates the pancreatic acinar cell expression of Atp2c2, the gene encoding secretory pathway calcium ATPase 2

The platinum (II) complex [Pt(O,O′-acac)(γ-acac)(DMS)] alters the intracellular calcium homeostasis in MCF-7 breast cancer cells

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