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Lingnan Modern Clinics in Surgery ›› 2019, Vol. 19 ›› Issue (01): 28-33.DOI: 10.3969/j.issn.1009-976X.2019.01.006

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LncRNA SNHG7 promote proliferation and metastasis of breast cancer through regulating β?catenin

ZHANG Ruihua, LAO Weisi, XU Ying, CAI Donghao, BI Zuofei, DUAN Chaohui.   

  1. Department of Clinical Laboratory, Sun Yat?sen Memorial Hospital, Sun Yat?sen University, Guangzhou 510120, China
  • Contact: DUAN Chaohui

LncRNA SNHG7通过调控β?catenin蛋白影响乳腺癌细胞的增值、迁移和侵袭

张瑞华, 劳伟思, 许英, 蔡栋昊, 毕卓菲, 段朝晖*   

  1. 中山大学孙逸仙纪念医院检验科,广州 510120
  • 通讯作者: 段朝晖

Abstract: [Abstract] Objective To explore the function and mechanism of long noncoding RNA SNHG7 in breast cancer. Methods qRT?PCR was to detect the expression of lncRNA SNHG7 in breast cancer in vitro. Cellular fractionation was to identify the subcellular localization of SNHG7 in MDA?MB?231.Si?SNHG7 was transfected into MDA?MB?231,and the effect of SNHG7 on the proliferation of breast cancer cell was measured by MTS assay and plate cloning assay. Wound healing and transwell assays were used to detect the effect of SNHG7 on the migratory and invasive ability of MDA?MB?231 cell. Expression changes of β?catenin and p?β?catenin protein after siSNHG7 intervention were measured by WB. Results SNHG7 over?expressed in breast cancer(P<0.05). After the siSNHG7 transfection,breast cancer cells proliferation(P<0.05), invasion and metastasis were inhibited(P<0.05). Furthermore, after the siSNHG7 intervention, the expression of β?catenin,C?Myc and CyclinD1 decreased significantly and p?β?catenin increased significantly. Conclusion The expression of SNHG7 in breast cancer is significantly up?regulated. After the siSNHG7 intervention, SNHG7 could partly inhibit the proliferation, invasion and metastasis of breast cancer by regulating the expression of β?catenin and p?β?catenin.

Key words: lncRNA SNHG7, invasive, cell proliferation, β?catenin, breast cancer

摘要: [摘要] 目的 探讨长链非编码RNA SNHG7(LncRNA SNHG7)在乳腺癌细胞系中的功能及其机制。方法 RT?qPCR检测LncRNA SNHG7在乳腺癌组织和乳腺癌细胞系的表达水平,核浆分离实验检测LncRNA SNHG7在乳腺癌细胞系MDA?MB?231中的定位。在MDA?MB?231细胞系中,siRNA 沉默LncRNA SNHG7后,利用MTS和平板克隆形成实验研究LncRNA SNHG7对细胞增殖的影响;利用划痕和transwell实验研究LncRNA SNHG7对细胞侵袭迁移的影响。通过Western blot(WB)实验研究LncRNA SNHG7在乳腺癌细胞系中可能参与的分子机制。结果 qPCR结果显示,与癌旁组织相比,LncRNA SNHG7在乳腺癌组织中高表达(P<0.05);与乳腺正常上皮MCF?10A相比,LncRNA SNHG7在乳腺癌细胞系中高表达。siRNA沉默LncRNA SNHG7后,细胞增殖能力和平板克隆形成能力被抑制(P<0.05),划痕实验显示细胞的愈合能力降低(P<0.05),transwell实验显示细胞的迁移和侵袭能力均被抑制(P<0.05)。WB结果显示β?catenin、C?Myc和CyclinD1蛋白的表达下调,磷酸化的β?catenin(p?β?catenin)蛋白降解增加。结论 LncRNA SNHG7在乳腺癌组织和乳腺癌细胞系中高表达。沉默LncRNA SNHG7后,细胞的增殖和侵袭迁移能力均降低。WB结果表明LncRNA SNHG7调控乳腺癌细胞的增殖和侵袭迁移可能与β?catenin蛋白的表达下调和p?β?catenin蛋白降解增加有关。

关键词: 乳腺癌, 增值, 侵袭, β?catenin, LncRNA SNHG7

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