Store-operated Ca2+ channels in prostate cancer epithelial cells: function, regulation, and role in carcinogenesis

Abeele, Fabien Vanden; Shuba, Yaroslav; Roudbaraki, Morad; Lemonnier, Loïc; Vanoverberghe, Karine; Mariot, Pascal; Skryma, Roman; Prevarskaya, Natalia

doi:10.1016/s0143-4160(03)00049-6

Cited by 99 publications

(30 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Upon refilling of the stores and termination of CIF production, CaM binds to iPLA 2 and inhibits it, and the activity of SOC and SOCE is halted. Consistent with a major role of iPLA 2 , a growing number of studies demonstrated that its irreversible inhibition impairs SOCE in different cell types (2)(3)(4)(5)(6)(7)(8)(9). However, no detailed study of CIF-iPLA 2 -dependent mechanism has been done in the cells in which SOCE is mediated by a highly Ca 2ϩ -selective SOC (historically called CRAC) (10).…”

Section: From the Boston University School Of Medicine Boston Massamentioning

confidence: 75%

Activation Mechanism for CRAC Current and Store-operated Ca2+ Entry

Csutora

Zarayskiy

Peter

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

2؉ release (net loss) as well as by simple buffering of free Ca 2؉ within the stores, 2) a specific 82-kDa variant of iPLA 2 ␤ and its corresponding activity are present in membrane fraction of RBL cells, 3) exogenous CIF (extracted from other species) mimics the effects of endogenous CIF and activates iPLA 2 ␤ when applied to cell homogenates but not intact cells, 4) activation of I CRAC can be triggered in resting RBL cells by dialysis with exogenous CIF, 5) molecular or functional inhibition of iPLA 2 ␤ prevents activation of I CRAC , which could be rescued by cell dialysis with a human recombinant iPLA 2 ␤, 6) dependence of I CRAC on intracellular pH strictly follows pH dependence of iPLA 2 ␤ activity, and 7) (S)-BEL, a chiral enantiomer of suicidal substrate specific for iPLA 2 ␤, could be effectively used for pharmacological inhibition of I CRAC and store-operated Ca 2؉ entry. These findings validate and significantly advance our understanding of the CIF-iPLA 2 -dependent mechanism of activation of I CRAC and store-operated Ca 2؉ entry.

show abstract

Section: From the Boston University School Of Medicine Boston Massamentioning

confidence: 75%

Activation Mechanism for CRAC Current and Store-operated Ca2+ Entry

Csutora

Zarayskiy

Peter

et al. 2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…In addition to the TRPM isoforms described above (TRPM1, TRPM5, and TRPM8; see the Introduction), in cultured pulmonary arterial myocytes, a close parallelism has been found between the expression level of TRPC1, the magnitude of endogenous store-operated Ca 2+ entry (SOC), and the rate of serum-dependent cell growth, where antisense elimination of TRPC1 reduces the growth rate with a concomitant decrease in SOC activity (37). A similar significance of SOC activity and involvement of TRPC1 and TRPV6 (or CaTL) has been suggested for the aberrant cell growth in a prostate cancer cell line LNCaP (38,39).…”

Section: +mentioning

confidence: 78%

Involvement of TRPM7 in Cell Growth as a Spontaneously Activated Ca2+ Entry Pathway in Human Retinoblastoma Cells

et al. 2004

View full text Add to dashboard Cite

Abstract.We investigated the possible involvement of the melastatin family protein TRPM7 in Ca 2+-mediated proliferative control of human retinoblastoma (RB) cells. , LOE908, 2-APB) suppressed the spontaneous Ca 2+ influx and decelerated the growth of RB cells with similar efficacies. Excision of the RB cell membrane (inside-out) into MgATP-free solution induced a 70pS single channel activity, which was effectively inhibited by millimolar concentrations of Mg 2+ or MgATP. RT-PCR and immunocytochemical experiments revealed the expression of TRPM7 mRNA and protein in RB cells, and heterologous expression of TRPM7 in HEK293 cells reproduced the key features of I spont . In contrast, elimination of this protein from RB cells by siRNA silencing markedly reduced I spont density and the magnitude of spontaneous Ca 2+ influx, which was paralleled by decreased TRPM7 immunoreactivity, decelerated cell proliferation, and retarded G 1 / S cell cycle progression. These results suggest a significant regulatory role of TRPM7 for RB cell proliferation as a spontaneously activated Ca 2+ influx pathway.

show abstract

“…The inhibition of Ca 2+ store pumps in human prostate LNCaP cells inhibits the proliferation as well as the transition to androgen independence (Abeele et al 2003). In the present study, the exposure of DU-145 cells to 250μM BA significantly reduced NAD + -induced cytoplasmic Ca 2+ transients, and 1,000μM BA completely abolished them (Fig.…”

Section: Discussionmentioning

confidence: 99%

Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells

et al. 2008

View full text Add to dashboard Cite

Boron (B) is a developmental and reproductive toxin. It is also essential for some organisms. Plants use uptake and efflux transport proteins to maintain homeostasis, and in humans, boron has been reported to reduce prostate cancer. Ca2+ signaling is one of the primary mechanisms used by cells to respond to their environment. In this paper, we report that boric acid (BA) inhibits NAD+ and NADP+ as well as mechanically induced release of stored Ca2+ in growing DU-145 prostate cancer cells. Cell proliferation was inhibited by 30% at 100 microM, 60% at 250 microM, and 97% at 1,000 microM BA. NAD+-induced Ca2+ transients were partly inhibited at 250 microM BA and completely at 1,000 microM BA, whereas both NADP+ and mechanically induced transients were inhibited by 1,000 microM BA. Expression of CD38 protein increased in proportion to BA exposure (0-1,000 microM). In vitro mass spectrometry analysis showed that BA formed adducts with the CD38 products and Ca2+ channel agonists cyclic adenosine diphosphate ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP). Vesicles positive for the Ca2+ fluorophore fluo-3 acetoxymethyl ester accumulated in cells exposed to 250 and 1,000 microM BA. The BA analog, methylboronic acid (MBA; 250 and 1,000 microM), did not inhibit cell proliferation or NAD+, NADP+, or mechanically stimulated Ca2+ store release. Nor did MBA increase CD38 expression or cause the formation of intracellular vesicles. Thus, mammalian cells can distinguish between BA and its synthetic analog MBA and exhibit graded concentration-dependent responses. Based on these observations, we hypothesize that toxicity of BA stems from the ability of high concentrations to impair Ca2+ signaling.

show abstract

Store-operated Ca2+ channels in prostate cancer epithelial cells: function, regulation, and role in carcinogenesis

Cited by 99 publications

References 73 publications

Activation Mechanism for CRAC Current and Store-operated Ca2+ Entry

Activation Mechanism for CRAC Current and Store-operated Ca2+ Entry

Involvement of TRPM7 in Cell Growth as a Spontaneously Activated Ca2+ Entry Pathway in Human Retinoblastoma Cells

Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells

Contact Info

Product

Resources

About