[Intermediate-conductance-Ca2+-activated K+ channels are overexpressed in endometrial cancer and involved in regulating proliferation of endometrial cancer cells].
[Intermediate-conductance-Ca2+-activated K+ channels are overexpressed in endometrial cancer and involved in regulating proliferation of endometrial cancer cells].
复制标题
中电导Ca2激活K通道在子宫内膜癌中过度表达并参与调节子宫内膜癌细胞的增殖。
DOI：
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发表时间：
2007
期刊：
影响因子：
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通讯作者：
X. Yi
中科院分区：
文献类型：
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作者：
Zhen;You;Min Su;X. Yi
目的
目的研究中电导钙激活钾通道（IKCa 1）在子宫内膜癌中的表达及其对子宫内膜癌细胞增殖的调节作用。
方法
采用Western blot和RT-PCR检测13例正常子宫内膜和25例子宫内膜癌组织中IKCa 1通道的表达，并采用RNA干扰、[（3）H]胸苷掺入和IKCa 1通道抑制剂等方法探讨IKCa 1通道在子宫内膜癌细胞HEC-1A增殖调控中的作用。
结果
IKCa 1 mRNA在子宫内膜癌组织中的表达率（84%，0.89 ± 0.52）明显高于正常子宫内膜组织（8%，0.14 ± 0.12; P < 0.01）。IKCa 1蛋白在子宫内膜癌组织中的表达率（80%，1.18 ± 0.41）明显高于正常子宫内膜组织（15%，0.71 ± 0.26; P < 0.01）。克霉唑是IKCa 1通道的抑制剂，已知其抑制IKCa 1通道的功能，引起HEC-1A细胞数量的时间和剂量依赖性减少。Western印迹分析显示，转染靶IKCa 1小干扰RNA（siRNA）的细胞的完整裂解物中IKCa 1水平与转染前相比显著降低。（48.27 ± 9.07）%的非沉默RNA转染细胞;转染靶IKCa 1 siRNA的HEC-1A细胞中[（3）H]胸苷掺入也减少，siRNA抑制HEC-1A细胞增殖，与转染非沉默RNA的细胞相比，差异有统计学意义（P < 0.05）。
结论
IKCa 1通道的表达可能与子宫内膜癌的增殖密切相关，下调其表达可能抑制其发展。
OBJECTIVE
To study the expression of intermediate-conductance-Ca(2+)-activated K(+) (IKCa1) channels in endometrial cancer and its role in regulating proliferation of endometrial cancer cells.
METHODS
Western blot and RT-PCR were used to examine the expression of IKCa1 channels in 13 normal endometrial specimens and 25 endometrial cancer specimens; and RNA interference (RNAi), [(3)H] thymidine incorporation, and inhibitor of IKCa1 channel were used to explore the role of IKCa1 channels in regulation of proliferation of endometrial cancer cells HEC-1A.
RESULTS
The expression rate and level of IKCa1 mRNA in endometrial carcinoma (84%, 0.89 +/- 0.52) were higher than in normal endometria (8%, 0.14 +/- 0.12; P < 0.01). The expression rate and level of IKCa1 protein in endometrial carcinomas (80%, 1.18 +/- 0.41) were higher than in normal endometria (15%, 0.71 +/- 0.26; P < 0.01). Clotrimazole, an inhibitor of IKCa1 channels known to suppress the function of the channels, caused a both time- and dose-dependent decrease in cell number of HEC-1A cell. Western blot analysis revealed that the IKCa1 level in whole lysates of the cells transfected with target-IKCa1 small interference RNA (siRNA) was (48.27 +/- 9.07)% of that found in the cells transfected with non-silencing RNA; [(3)H] thymidine incorporation in HEC-1A cells transfected with target-IKCa1 siRNA was also reduced, siRNA inhibited HEC-1A cell proliferation, compared with the cells transfected with non-silencing RNA (P < 0.05).
CONCLUSION
The expression of IKCa1 channels may be closely related to the proliferation of endometrial cancer, and down regulation of its expression may suppress its development.