کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3946544 1254344 2007 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Voltage-gated K+ channels are associated with cell proliferation and cell cycle of ovarian cancer cell
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی زنان، زایمان و بهداشت زنان
پیش نمایش صفحه اول مقاله
Voltage-gated K+ channels are associated with cell proliferation and cell cycle of ovarian cancer cell
چکیده انگلیسی

ObjectivesTo study the role of Voltage-gated potassium ion channels (Kv) in cell proliferation and cell cycle of ovarian cancer cell.MethodsThe effects of voltage-gate K+ channels on human ovarian cancer cell line (A2780 cell) proliferation and cell cycle were observed by means of MTT and flow cytometry. A variety of K+ channel blockers were used in order to differentiate the critical subtype of K+ channels involved. Mechanism of K+ channel in cell proliferation was explored by studying the relationship between the K+ channel and Ca2+ entry. Kv and L-type Ca2+ channel gene expressions were determined by RT-PCR.Results4-Aminopyridine, an inhibitor of voltage-gated K+ channels, significantly inhibited the proliferation of A2780 cells as measured by MTT. 4-Aminopyridine also significantly affected the cell cycle, which increased the percentage of cells in G0/G1, and reduced the percentage of cells in S phase and G2/M phase. Non-selective K+ channel blockers tetrapentylammonium (TPeA) and verapamil had similar inhibitory effects on A2780 cell proliferation and cell cycle. In contrast, iberiotoxin, a selective inhibitor of KCa channels, and glibenclamide, a potent inhibitor of KATP channels, had no effect on the cell proliferation and cell cycle of A2780. Moreover K+ channels inhibitor, TPeA and verapamil, can blocked Ca2+ influx in these cells.ConclusionVoltage-gated K+ channels play an important role in the proliferation and cell cycle of ovarian cancer cell. It is likely that the influence of Kv channels on A2780 cell proliferation and cell cycle is mediated by a Ca2+-dependent mechanism.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gynecologic Oncology - Volume 104, Issue 2, February 2007, Pages 455–460
نویسندگان
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