Consequences of activating the calcium-permeable ion channel TRPV1 in breast cancer cells with regulated TRPV1 expression

Wu, Tina T. L., Peters, Amelia A., Tan, Ping T., Roberts-Thomson, Sarah J. and Monteith, Gregory R. (2014) Consequences of activating the calcium-permeable ion channel TRPV1 in breast cancer cells with regulated TRPV1 expression. Cell Calcium, 56 2: 59-67. doi:10.1016/j.ceca.2014.04.006

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Author Wu, Tina T. L.
Peters, Amelia A.
Tan, Ping T.
Roberts-Thomson, Sarah J.
Monteith, Gregory R.
Title Consequences of activating the calcium-permeable ion channel TRPV1 in breast cancer cells with regulated TRPV1 expression
Journal name Cell Calcium   Check publisher's open access policy
ISSN 1532-1991
0143-4160
Publication date 2014-08
Year available 2014
Sub-type Article (original research)
DOI 10.1016/j.ceca.2014.04.006
Open Access Status File (Author Post-print)
Volume 56
Issue 2
Start page 59
End page 67
Total pages 9
Place of publication London, United Kingdom
Publisher Churchill Livingstone
Collection year 2015
Language eng
Abstract Increased expression of specific calcium channels in some cancers and the role of calcium signaling in proliferation and invasion have led to studies assessing calcium channel inhibitors as potential therapies for some cancers. The use of channel activators to promote death of cancer cells has been suggested, but the risk of activators promoting cancer cell proliferation and the importance of the degree of channel over-expression is unclear. We developed an MCF-7 breast cancer cell line with inducible TRPV1 overexpression and assessed the role of TRPV1 levels on cell death mediated by the TRPV1 activator capsaicin and the potential for submaximal activation to promote proliferation. The TRPV1 level was a determinant of cell death induced by capsaicin. A concentration response curve with varying TRPV1 expression levels identified the minimum level of TRPV1 required for capsaicin induced cell death. At no level of TRPV1 over-expression or capsaicin concentration did TRPV1 activation enhance proliferation. Cell death induced by capsaicin was necrotic and associated with up-regulation of c-Fos and RIP3. These studies suggest that activators of specific calcium channels may be an effective way to induce necrosis and that this approach may not always be associated with enhancement of cancer cell proliferation.
Keyword Breast cancer
Calcium, necrosis
TRPV1
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Pharmacy Publications
 
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