Table 1.
Ca2+channel | Cell type | Mechanisms and effectors | References |
---|---|---|---|
Store-dependent SOC channels | |||
STIM1-Orai1 |
• Human cervical cancer SiHa and CaSki cells |
• Increase in EGF-stimulated cellular migration and invasion |
[29,30] |
• Increase in focal adhesion dynamics through the Ca2+-regulated protease calpain and cytoplasmic kinase Pyk2 | |||
• Upregulation of EGF-induced MLC phosphorylation and actomyosin reorganization | |||
• Upregulation of VEGF production | |||
• Promotion of tumor growth and angiogenesis in a xenograft mice model | |||
|
• Human breast cancer MDA-MB-231 cells and mouse mammary tumor 4 T1 cells |
• Increase in serum-induced cellular migration and invasion |
[31] |
• Increase in focal adhesion turnover rates through Ras and Rac1 | |||
• Promotion of tumor growth and metastasis in a xenograft mice model | |||
STIM-Orai3 |
• Human breast cancer MCF7 cells (ER+ breast cancer cells) |
• Increase in anchorage-independent growth and Matrigel invasion |
[32,33] |
|
|
• Increase in tumorigenesis in a xenograft mice model |
|
Store-independent SOC channel | |||
SPCA2-Orai1 |
• Human breast cancer MCF-7 cells |
• Constitutively active store-independent Ca2+ influx |
[34] |
• Promotion of proliferation and colony formation | |||
|
|
• Increase in tumorigenesis in a xenograft mice model |
|
TRP channels | |||
TRPM1 |
• Murine melanoma B16-F1 cells |
• Reduce in tumor metastasis |
[35,36] |
TRPM7 |
• Human breast cancer MDA-MB-231 cells and MEF cells |
• Increase in cellular migration |
[18,37-39] |
• Guidance of polarized cellular migration | |||
• Increase in peripheral focal adhesion turnovers through the Ca2+-regulated protease m-calpain | |||
• Inhibition of myosin II-based cell contractility | |||
• Increase in tumorigenesis in a xenograft mice model | |||
|
• Human nasopharyngeal cancer 5-8 F and 6-10B cells |
• Increase in cellular migration |
[40] |
|
• Human lung cancer A549 cells |
• Increase in EGF-stimulated cellular migration |
[38] |
TRPM8 |
• Human prostate cancer PC-3 cells |
• Decrease in cellular migration |
[41,42] |
• Inactivation of FAK | |||
TRPV1 |
• Human hepatoblastoma HepG2 cells |
• Increase in HGF-stimulated cellular migration |
[43,44] |
TRPV2 |
• Human prostate cancer LNCaP and PC-3 cells |
• Increase in cellular migration and invasion |
[45] |
• Induction of invasive enzymes MMP-2, MMP-9 and cathepsin B | |||
• Increase in tumorigenesis in a xenograft mice model | |||
TRPC6 |
• Human glioblastoma cells |
• Increase in cell proliferation through regulation of CDK1 activation and Cdc25C expression |
[46,47] |
• Increase in anchorage-independent growth and Matrigel invasion | |||
• Increase in endothelial cell tube formation | |||
• Increase in tumorigenesis in a xenograft mice model |
Cdc25C, cell division cycle 25 homolog C; CDK1, cyclin-dependent kinase 1; EGF, epidermal growth factor; ER, estrogen receptor; FAK, focal adhesion kincase; HGF, hepatocyte growth factor; SPCA2, secretory pathway Ca2+-ATPase; MEF, mouse embryonic fibroblast; MMP, matrix metalloproteinase; Pyk2, proline-rich tyrosine kinase 2; VEGF, vascular endothelial cell growth factor.