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F. Lu, H. Chen, C. Zhou, S. Liu, M. Guo, P. Chen, H. Zhuang, D. Xie and S. Wu, “T-Type Ca(2+) Channel Expression in Human Esophageal Carcinomas: A Functional Role in Proliferation,” Cell Calcium, Vol. 43, No. 1, 2008, pp. 49-58. doi:10.1016/j.ceca.2007.03.006
has been cited by the following article:
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TITLE:
Exploiting MCF-7 Cells’ Calcium Dependence with Interlaced Therapy
AUTHORS:
Jonathan Pottle, Chengrong Sun, Lloyd Gray, Ming Li
KEYWORDS:
Breast Cancer; Calcium; Calcium Channel Blockers; Ion Channels; Interlaced Therapy
JOURNAL NAME:
Journal of Cancer Therapy,
Vol.4 No.7A,
July
22,
2013
ABSTRACT: The purpose of this study is to demonstrate MCF-7 cells’ dependence on calcium for growth and to exploit that dependence to improve chemotherapy efficacy. Fura-2 fluorescence imaging shows that MCF-7 cells maintain a higher basal intracellular calcium concentration than non-tumorigenic MCF-10A cells. Blocking T-type calcium channels with mibefradil reduced MCF-7 intracellular calcium concentration. Flow cytometry shows that knocking down T-type calcium channel expression with siRNA caused an increase in MCF-7 cells in G1 phase and a decrease in cells in S phase. Proliferation assays of MCF-7 cells treated with EGTA and thapsigargin reveal the dependence of MCF-7 cell growth on extracellular and intracellular calcium sources, respectively. In vitro, interlaced treatment that alternated the T-type calcium channel blocker NNC-55-0396 with paclitaxel more effectively reduced MCF-7 cell number than chemotherapy alone. In a mouse in vivo model, interlaced mibefradil and paclitaxel more effectively reduced MCF-7 xenograft size than chemotherapy alone. These findings indicate that MCF-7 cells are dependent on calcium for proliferation, particularly in passing the G1/S cell cycle checkpoint. Further, this dependence on calcium can be exploited by alternating treatment with T-type calcium channel blockers with paclitaxel in an interlaced therapy scheme that increases the efficacy of the chemotherapy.