miR-34c对II型子宫内膜癌HEC-1-B细胞生长和凋亡的影响

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摘要目的：研究miR-34c对Ⅱ型子宫内膜癌HEC-1-B细胞的生长及凋亡的影响。方法：用hsa-miR-34c mimics转染HEC-1-B细胞。流式细胞技术测定细胞转染率，实时荧光定量PCR验证转染后miR-34c的表达。CCK-8检测细胞增殖能力的改变。细胞克隆形成实验观察miR-34c对细胞生长的长期抑制。流式细胞技术测细胞凋亡。结果：细胞转染率为81.16%。相对于对照组，转染后实验组miR-34c表达明显增加，细胞增殖、克隆形成能力减弱，凋亡增加（P＜0.05）。结论：miR-34c能明显抑制Ⅱ型子宫内膜癌细胞的增殖，促进细胞凋亡，是Ⅱ型子宫内膜癌的潜在抑癌基因。

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	李甫钥
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	郑飞云

关键词 ： miR-34c, Ⅱ型子宫内膜肿瘤, 细胞, 增殖, 凋亡

Abstract：Objective: To investigate the effect miR-34c on the growth and apoptosis of type II endometrial carcinoma cells (HEC-1-B cell line). Methods: Up-regulated the expression of miR-34c by transfecting cells with hsa-miR-34c mimics, the transfection efficiency was detected by flow cytometry and further verified by quantitative real-time PCR (qRT-PCR). Cell proliferation assay by CCK-8 and colony formation assay applied to demonstrate that miR-34c could inhibit the growth of HEC-1-B cells. Cells apoptosis assay was analyzed by flow cytometry. Results: The transfection efficiency was 81.16%. The overexpression of miR-34c (detected by qRT-PCR) could inhibit cell proliferation, colony formation and promote cells apoptosis (P<0.05). Conclusion: MiR-34c can inhibit the growth and promote apoptosis of HEC-1-B cells significantly, and function is a potential tumor suppressor in type II endometrial carcinoma.

Key words： miR-34c type II endometrial carcinoma cell proliferation apoptosis

收稿日期: 2013-09-25

基金资助:浙江省自然科学基金资助项目（Y2090699）

通讯作者: 郑飞云，主任医师，硕士生导师，Email：zfy5710 @163.com。

作者简介: 李甫钥（1989-），男，浙江苍南人，硕士生

链接本文:

https://xb.wmu.edu.cn/CN/ 或 https://xb.wmu.edu.cn/CN/Y2014/V44/I2/86

[1] Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012[J].CA Cancer J Clin, 2012, 62(1): 10-29.

[2] Ueda SM, Kapp DS, Cheung MK, et al. Trends in demo-graphic and clinical characteristics in women diagnosed with corpus cancer and their potential impact on the increasing number of deaths[J]. Am J Obstet Gynecol, 2008, 198(2):218.e1-218.e6.

[3] Bokhman JV. Two pathogenetic types of endometrial carcinoma[J]. Gynecol Oncol, 1983, 15(1): 10-17.

[4] Tergas AI, Buell-Gutbrod R, Gwin K, et al. Clinico-patho-logic comparison of type II endometrial cancers based on tamoxifen exposure[J]. Gynecol Oncol, 2012, 127(2): 316-320.

[5] Bartel DP. MicroRNAs: genomics, biogenesis, mechanism,and function[J]. Cell, 2004, 116(2): 281-297.

[6] Esquela-Kerscher A, Slack FJ. Oncomirs - microRNAs witha role in cancer[J]. Nat Rev Cancer, 2006, 6(4): 259-269.

[7] 薛纪森, 张乾, 李晓琳, 等. 子宫内膜癌I型和II型miRNA表达谱差异的分析[J]. 实用医学杂志, 2011, 27(22): 4051-4054.

[8] 孙蓬明, 魏丽惠, 高敏, 等. 雌激素受体相关受体α过度表达对雌激素受体阴性的子宫内膜癌细胞增殖的影响[J]. 中华妇产科杂志, 2007, 42(6): 408-411.

[9] Le XF, Merchant O, Bast RC, et al. The roles of microRNAs in the cancer invasion-metastasis cascade[J]. Cancer microenviron, 2010, 3(1): 137-147.

[10] Bommer GT, Gerin I, Feng Y, et al. p53-mediated activation of miRNA34 candidate tumor-suppressor genes[J]. Curr Biol, 2007, 17(15): 1298-1307.

[11] Son MS, Jang MJ, Jeon YJ, et al. Promoter polymorphisms of pri-miR-34b/c are associated with hepatocellular carcinoma[J]. Gene, 2013, 524(2): 156-160.

[12] Wong MY, Yu Y, Walsh WR, et al. microRNA-34 family and treatment of cancers with mutant or wild-type p53 (Review)[J]. Int J Oncol, 2011, 38(5): 1189-1195.

[13] Yeramian A, Moreno-Bueno G, Dolcet X, et al. Endometrial carcinoma: molecular alterations involved in tumor devel-opment and progression[J]. Oncogene, 2013, 32(4): 403-413.

[14] Mendivil A, Schule K, Gehrig P, et al. Non-endometrioidadenocarcinoma of the uterine corpus: a review of selected histological subtypes[J]. Cancer Control, 2009, 16(1): 46-52.

[15] Tanaka N, Toyooka S, Soh J, et al. Downregulation ofmicroRNA-34 induces cell proliferation and invasion ofhuman mesothelial cells[J]. Oncol Rep, 2013, 29(6): 2169-2174.