Open AccessCalcium signaling and T-type calcium channels in cancer cell cycling
Author(s) -
James T. Taylor,
Xianyi Zeng,
Jonathan E. Pottle,
Kevin Lee,
Alun R. Wang,
Stephenie G Yi,
Jennifer A S Scruggs,
Suresh S Sikka,
Ming Li
Publication year - 2008
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.14.4984
Subject(s) - t type calcium channel , microbiology and biotechnology , cell growth , calcium , cell cycle , calcium channel , calcium signaling , voltage dependent calcium channel , calcium in biology , mitosis , intracellular , cancer cell , chemistry , cell type , signal transduction , cell , biology , cancer , biochemistry , genetics , organic chemistry
Regulation of intracellular calcium is an important signaling mechanism for cell proliferation in both normal and cancerous cells. In normal epithelial cells, free calcium concentration is essential for cells to enter and accomplish the S phase and the M phase of the cell cycle. In contrast, cancerous cells can pass these phases of the cell cycle with much lower cytoplasmic free calcium concentrations, indicating an alternative mechanism has developed for fulfilling the intracellular calcium requirement for an increased rate of DNA synthesis and mitosis of fast replicating cancerous cells. The detailed mechanism underlying the altered calcium loading pathway remains unclear; however, there is a growing body of evidence that suggests the T-type Ca(2+) channel is abnormally expressed in cancerous cells and that blockade of these channels may reduce cell proliferation in addition to inducing apoptosis. Recent studies also show that the expression of T-type Ca(2+) channels in breast cancer cells is proliferation state dependent, i.e. the channels are expressed at higher levels during the fast-replication period, and once the cells are in a non-proliferation state, expression of this channel is minimal. Therefore, selectively blocking calcium entry into cancerous cells may be a valuable approach for preventing tumor growth. Since T-type Ca(2+) channels are not expressed in epithelial cells, selective T-type Ca(2+) channel blockers may be useful in the treatment of certain types of cancers.