中国医科大学学报

中国医科大学学报
  • 中文核心期刊
  • 中国科技核心期刊
  • 中国高校百佳科技期刊
  • BA、CA收录

中国医科大学学报 ›› 2019, Vol. 48 ›› Issue (2): 124-127.doi: 10.12007/j.issn.0258-4646.2019.02.007

• 论著 • 上一篇    下一篇

跨膜蛋白16F对乳腺癌细胞增殖及迁移的影响

樊璐, 王慧, 肖庆桓   

  1. 中国医科大学药学院离子通道药理学研究室, 沈阳 110122
  • 收稿日期:2018-10-23 出版日期:2019-02-28 发布日期:2019-01-05
  • 通讯作者: 肖庆桓 E-mail:qinghuanxiao12345@163.com
  • 作者简介:樊璐(1992-),女,硕士研究生.
  • 基金资助:
    国家自然科学基金(81572613,81702611)

Effects of TMEM16F on the Proliferation and Migration of Breast Cancer Cells

FAN Lu, WANG Hui, XIAO Qinghuan   

  1. Department of Ion Channel Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, China
  • Received:2018-10-23 Online:2019-02-28 Published:2019-01-05

摘要: 目的 探讨跨膜蛋白16F(TMEM16F)在乳腺癌细胞中的表达,阐明敲除TMEM16F对T47D乳腺癌细胞增殖和迁移的影响。方法 应用Western blotting检测MDA-MB-231、T47D乳腺癌细胞TMEM16F蛋白表达。应用CCK-8细胞增殖实验检测敲除TMEM16F对T47D乳腺癌细胞增殖的影响。应用细胞划痕实验检测敲除TMEM16F对T47D乳腺癌细胞迁移的影响。结果 Western blotting结果显示,在乳腺癌细胞中有TMEM16F蛋白表达。CCK-8细胞增殖实验结果显示,与Scrambled shRNA组比较,敲除TMEM16F后T47D乳腺癌细胞增殖能力降低(P=0.037 0)。划痕实验结果显示,与对照组比较,敲除TMEM16F后T47D乳腺癌细胞的迁移能力增强(P=0.002 7)。结论 TMEM16F在T47D乳腺癌细胞中高表达,敲除TMEM16F能够抑制T47D乳腺癌细胞增殖而促进T47D乳腺癌细胞迁移。

关键词: 乳腺癌, 跨膜蛋白16F, 增殖, 迁移

Abstract: Objective To investigate the expression of transmembrane protein 16F (TMEM16F) in breast cancer cells and to elucidate the effect of the knockdown of its gene on proliferation and migration of T47D breast cancer cells. Methods The expression of TMEM16F protein in MDA-MB-231 and T47D breast cancer cells was detected by Western blotting. The effect of TMEM16F knockdown on the proliferation of T47D breast cancer cells was detected by CCK-8 cell proliferation assay,and its effect on the migration of T47D breast cancer cells was examined by cell scratch assay. Results Western blotting results showed TMEM16F protein expression in breast cancer cells. The results of CCK-8 cell proliferation assay showed that compared to the Scrambled shRNA group,the proliferation of T47D breast cancer cells was decreased after TMEM16F knockdown (P=0.037 0). The results of the scratch test showed that the migration ability of T47D breast cancer cells was enhanced after TMEM16F knockdown,compared to the control group (P=0.002 7). Conclusion TMEM16F is highly expressed in T47D breast cancer cells. Knockdown of TMEM16F can inhibit the proliferation and promote the migration of T47D breast cancer cells.

Key words: breast cancer, transmembrane protein 16F, proliferation, migration

中图分类号: 

  • R966
[1] KUNZELMANN K,TIAN Y,MARTINS JR,et al. Anoctamins[J].Pflugers Arch,2011,462(2):195-208. DOI:10.1007/s00424-011-0975-9.
[2] TOSHIHIRO F,ASUKA S,SATOSHI N,et al. TMEM16F is required for phosphatidylserine exposure and microparticle release in activated mouse platelets[J]. Proc Natl Acad Sci USA,2015,112(41):12800-12805. DOI:10.1073/pnas.1516594112.
[3] GYOBU S,ISHIHARA K,SUZUKI J,et al. Characterization of the scrambling domain of the TMEM16 family[J]. Proc Natl Acad Sci USA,2017,114(24):6274-6279. DOI:10.1073/pnas.1703391114.
[4] SUZUKI J,UMEDA M,SIMS PJ,et al. Calcium-dependent phospholipid scrambling by TMEM16F[J]. Nature,2010,468(7325):834-838. DOI:10.1038/nature09583.
[5] LIU G,LIU G,CHEN H,et al. Involvement of Ca2+ activated Cl-channel Ano6 in platelet activation and apoptosis[J]. Cell Physiol Biochem,2015,37(5):1934-1944. DOI:10.1159/000438554.
[6] SCHENK LK,SCHULZE U,HENKE S,et al. TMEM16F regulates baseline phosphatidylserine exposure and cell viability in human embryonic kidney cells[J]. Cell Physiol Biochem,2016,38(6):2452-2463. DOI:10.1159/000445596.
[7] YANG H,KIM A,DAVID T,et al. TMEM16F forms a Ca2+-activated cation channel required for lipid scrambling in platelets during blood coagulation[J]. Cell,2012,151(1):111-122. DOI:10.1016/j.cell.2012.07.036.
[8] GRUBB S,POULSEN KA,JUUL CA,et al. TMEM16F (Anoctamin 6),an anion channel of delayed Ca2+ activation[J]. J Gen Physiol,2013,141(5):585-600. DOI:10.1085/jgp.201210861.
[9] GALINDO BE,VACQUIER VD. Phylogeny of the TMEM16 protein family:some members are overexpressed in cancer[J]. Inter J Mol Med,2005,16(5):919-924. DOI:10.1089/hum.2005.16.1346.
[10] YU K,WHITLOCK JM,LEE K,et al. Identification of a lipid scrambling domain in ANO6/TMEM16F[J]. elife,2015,4:e06901. DOI:10.7554/eLife.06901.
[11] AKERVALL JA,JIN Y,WENNERBERG JP,et al. Chromosomal abnormalities involving 11q13 are associated with poor prognosis in patients with squamous cell carcinoma of the head and neck[J]. Cancer,1995,76(5):853-859.
[12] JACOBSEN KS,ZEEBERG K,SAUTER DR,et al. The role of TMEM16A (ANO1) and TMEM16F (ANO6) in cell migration[J]. Pflugers Archiv,2013,465(12):1753-1762. DOI:10.1007/s00424-013-1315-z.
[13] BRITSCHGI A,BILL A,BRINKHAUS H,et al. Calcium-activated chloride channel ANO1 promotes breast cancer progression by activating EGFR and CAMK signaling[J]. Proc Natl Acad Sci USA,2013,110(11):E1026-E1034. DOI:10.1073/pnas.1217072110.
[14] WU H,WANG H,GUAN S,et al. Cell-specific regulation of proliferation by Ano1/TMEM16A in breast cancer with different ER,PR,and HER2 status[J]. Oncotarget,2017,8(49):84996-85013. DOI:10.18632/oncotarget.18662.
[15] STANICH JE,GIBBONS SJ,EISENMAN ST,et al. Ano1 as a regulator of proliferation[J]. Am J Physiol Gastroint Liver Physiol,2011,301(6):G1044-G1051. DOI:10.1152/ajpgi.00196.2011.
[16] ZHAO P,TORCASO A,MARIANO A,et al. Anoctamin 6 regulates C2C12 myoblast proliferation[J]. PLos One,2014,9(3):e92749. DOI:10.1371/journal.pone.0092749.
[17] AKTAS B,KASIMIR-BAUER S,MÜLLER V,et al. Comparison of the HER2,estrogen and progesterone receptor expression profile of primary tumor,metastases and circulating tumor cells in metastatic breast cancer patients[J]. BMC Cancer,2016,16:522. DOI:10.1186/s12885-016-2587-4.
[1] 王子文, 刘兆玉. miR-510通过打靶c-MYC抑制肝细胞癌的发展[J]. 中国医科大学学报, 2019, 48(4): 300-304.
[2] 庄莹, 张淑红, 樊伟平, 赵小芳, 孙海燕, 刘爽, 张虎. 乳腺癌中DEAH盒解旋酶16的表达及临床意义[J]. 中国医科大学学报, 2019, 48(4): 305-308.
[3] 蔡存伟, 温媛媛, 李晓燕, 张丽娜. SIAH1核异位表达抑制乳腺癌细胞凋亡的作用机制[J]. 中国医科大学学报, 2019, 48(4): 328-332,337.
[4] 何波, 王文瑞, 李健, 王平. 蛋白酶体抑制剂MG132对膀胱癌细胞增殖及凋亡的影响[J]. 中国医科大学学报, 2019, 48(4): 349-353.
[5] 高天, 余铃, 李舒, 刘佳勇, 白楚杰, 薛瑞峰, 张路, 方志伟, 樊征夫. Notch信号通路促进滑膜肉瘤细胞SW982增殖和侵袭的研究[J]. 中国医科大学学报, 2019, 48(3): 210-215.
[6] 赵越, 孙媛媛, 佟雪, 岳鹏杰, 富伟能. miR-362-3p在喉癌组织中的表达及其对喉癌Hep-2细胞迁移的影响[J]. 中国医科大学学报, 2019, 48(3): 236-239.
[7] 姜雪梅, 钱越, 戴红良. 染料木黄酮通过ERK及JNK通路抑制人非小细胞肺癌PC14细胞增殖[J]. 中国医科大学学报, 2019, 48(3): 274-276,280.
[8] 马金柱, 赵铁映, 刘明, 张瑞, 布日古德. 散发性乳腺癌与BRCA2基因rs206115位点多态性的相关分析[J]. 中国医科大学学报, 2019, 48(2): 149-152,158.
[9] 温行, 李章富, 王辉, 孙绍华, 郭星, 李福才. miR-200c调控肽基脯氨酰顺反异构酶对喉癌Hep-2细胞生物学行为的影响[J]. 中国医科大学学报, 2019, 48(1): 17-22,28.
[10] 李岩, 张德巍, 杨大业. 那可丁对人肺癌细胞A549生物学功能的影响[J]. 中国医科大学学报, 2019, 48(1): 66-70.
[11] 王黎明, 杨大业, 仇剑, 张德巍. miR-24对肺癌生物学功能的抑制作用[J]. 中国医科大学学报, 2019, 48(1): 71-74.
[12] 刘叶, 刘诗盈, 冯冬东, 李丽莉, 徐蕾, 王爱平. 内分泌治疗期间创新途径随访对提高乳腺癌患者自我效能和韧性水平的影响[J]. 中国医科大学学报, 2019, 48(1): 85-86.
[13] 杨帆, 陈英剑, 亓敏, 胡成进. 应用液体蛋白芯片-飞行时间质谱技术诊断乳腺癌的临床价值[J]. 中国医科大学学报, 2018, 47(6): 490-493,512.
[14] 宋起滨, 王哲, 王宇令, 李杨, 林爽. 脂肪源性干细胞促进大鼠神经施万细胞增殖和分泌功能[J]. 中国医科大学学报, 2018, 47(6): 527-531.
[15] 李忠华, 李慧峰, 李晓蕾. 瞬时感受器电位香草酸受体3促进胶质瘤U251细胞系增殖和侵袭[J]. 中国医科大学学报, 2018, 47(5): 394-397.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
[1] 邹飞, 任高伟, 周晓薇, 马艳萍, 齐莹, 阮强, 孙峥嵘. 人巨细胞病毒UL135蛋白结合蛋白的酵母双杂交筛选[J]. 中国医科大学学报, 2009, 38(9): 647 .
[2] 贺雪梅, 熊欣, 邹建中, 李发琪, 龚晓波. 超声消融剂量与生物学焦域特征[J]. 中国医科大学学报, 2009, 38(9): 654 .
[3] 高红, 吕良英, 白伟良, 王大佳, 黄英, 张志波, 王维林. 先天性巨结肠组织蛋白质组成分的双向凝胶电泳分析[J]. 中国医科大学学报, 2009, 38(10): 761 .
[4] 马秀岚, 李巍, 季文樾, 王宏伟, 边志刚, 顾兆伟. 先天性舌根囊肿的临床分析[J]. 中国医科大学学报, 2009, 38(12): 943 .
[5] 于雪馨, 王常林, 孙荣国, 杨屹. 鼠输尿管完全梗阻后肾脏病理及足细胞表型改变的研究[J]. 中国医科大学学报, 2010, 39(1): 1 .
[6] 王新利, 李卿, 高婷, 付立叶, 王扬, 蒋涛, 姜又红. 树突状细胞分泌的exosomes体外诱导特异性CTL抗肾癌的初步研究[J]. 中国医科大学学报, 2010, 39(1): 4 .
[7] 刁延娜, 马兰兰, 孟凡彪, 李宏图, 庞希宁. 骨髓间充质干细胞移植促进大鼠损伤脊髓的功能恢复[J]. 中国医科大学学报, 2010, 39(1): 7 .
[8] 张依宁, 魏敏杰, 孙明军. 伊立替康抑制人结直肠癌细胞增殖和ATP敏感性钾通道的相关性研究[J]. 中国医科大学学报, 2010, 39(1): 10 .
[9] 赵宇, 谢鹏, 朱晓峰, 蔡志友. 大鼠神经干细胞中MAPKK/MEK-MAPK/ERK信号转导通路的实验研究[J]. 中国医科大学学报, 2010, 39(1): 14 .
[10] 夏蒲, 徐小燕, 贾宝萍, 王薇, 关一夫, 高野康雄, 郑华川. 胃黏膜特异表达JC病毒T抗原质粒构建及表达鉴定[J]. 中国医科大学学报, 2010, 39(1): 18 .

中国医科大学学报版权所有©2018

未经允许,严禁擅自转载本站图文资料

地址:中国 沈阳市沈北新区蒲河路77号 110122

辽ICP备05014850

JOURNAL OF CHINA MEDICAL UNIVERSITY

ADDRESS: NO.77 PUHE ROAD

SHENYANG NORTH NEW AREA, SHENYANG

LIAONING PROVINCE, P.R. CHINA