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    岳成旭, 王文锐, 杨清玲, 陈昌杰. LncRNA SNHG15通过调控miRNA-451a促进乳腺癌细胞的上皮间质转化研究[J]. 蚌埠医科大学学报, 2022, 47(4): 421-425. DOI: 10.13898/j.cnki.issn.1000-2200.2022.04.001
    引用本文: 岳成旭, 王文锐, 杨清玲, 陈昌杰. LncRNA SNHG15通过调控miRNA-451a促进乳腺癌细胞的上皮间质转化研究[J]. 蚌埠医科大学学报, 2022, 47(4): 421-425. DOI: 10.13898/j.cnki.issn.1000-2200.2022.04.001
    shu
    YUE Cheng-xu, WANG Wen-rui, YANG Qing-ling, CHEN Chang-jie. Study on the LncRNA SNHG15 promoting the epithelial mesenchymal transformation of breast cancer cells by regulating miRNA-451a[J]. Journal of Bengbu Medical University, 2022, 47(4): 421-425. DOI: 10.13898/j.cnki.issn.1000-2200.2022.04.001
    Citation: YUE Cheng-xu, WANG Wen-rui, YANG Qing-ling, CHEN Chang-jie. Study on the LncRNA SNHG15 promoting the epithelial mesenchymal transformation of breast cancer cells by regulating miRNA-451a[J]. Journal of Bengbu Medical University, 2022, 47(4): 421-425. DOI: 10.13898/j.cnki.issn.1000-2200.2022.04.001
    shu

    LncRNA SNHG15通过调控miRNA-451a促进乳腺癌细胞的上皮间质转化研究

    Study on the LncRNA SNHG15 promoting the epithelial mesenchymal transformation of breast cancer cells by regulating miRNA-451a

      摘要
    • 摘要:
      目的研究长链非编码RNA小核仁RNA宿主基因15(LncRNA SNHG15)与miRNA-451a对乳腺癌细胞的生物学活性的影响。
      方法qRT-PCR法检测SNHG15、miRNA-451a及趋化因子受体4(CXCR4)在乳腺癌耐药细胞SKBR3-PR中的表达情况；细胞划痕实验检测干扰SNHG15及miRNA-451a抑制剂对SKBR3-PR的细胞迁移能力的影响；流式细胞术检测对细胞凋亡情况的影响；Western blotting实验检测CXCR4、上皮间质转化(EMT)相关蛋白Vimentin、Snail水平表达。
      结果相比于亲本细胞，乳腺癌耐药细胞株中SNHG15表达量上调，但差异无统计学意义(P>0.05), miRNA-451a表达量下降(P<0.05)，CXCR4表达量上调(P<0.01)；划痕实验结果显示SNHG15促进细胞的迁移(P<0.01), miRNA-451a可抑制细胞迁移(P<0.01)；细胞凋亡实验结果表明SNHG15抑制细胞凋亡(P<0.01)，miRNA-451a促进细胞凋亡(P<0.01)；Western blotting表明干扰SNHG15后，EMT相关蛋白Snail和CXCR4表达水平下降，miRNA-451a抑制剂组Snail和CXCR4表达水平上升(P<0.01)，Vimentin表达水平无统计学意义(P>0.05)。
      结论LncRNA SNHG15可能通过调控miRNA-451a促进乳腺癌细胞的迁移、凋亡，并且潜在调控CXCR4诱导乳腺癌细胞的EMT。

       

      Abstract:
      ObjectiveTo study the effects of leng noncoding RAN small nucleolar RNA host gene 15(LncRNA SNHG15) and microRNA-451a(miRNA-451a) on the biological activity of breast cancer cells.
      MethodsThe expression levels of SNHG15, miRNA-451a and chemokine receptor 4(CXCR4) in drug-resistant breast cancer SKBR3-PR cells were detected using qRT-PCR.The effects of the SNHG15 and miRNA-451a inhibitors on SKBR3-PR cells migration were determined by cell scratch assay.Flow cytometry was used to detect the apoptosis, and the protein expression levels of CXCR4, epithelial mesenchymal transformation(EMT)-related proteins Vimentin and Snail were detected by Western blotting.
      ResultsCompared with the parent cells, the expression level of miRNA-451a decreased(P<0.05), the expression level of CXCR4 was up-regulated in drug-resistant breast cancer cell lines(P<0.01).The results of cell scratch assay showed that the SNHG15 promoted cell migration(P<0.01), and the miRNA-451a inhibited cell migration(P<0.01).The results of apoptosis assay showed that the SNHG15 inhibited apoptosis(P<0.01) and the miRNA-451a promoted apoptosis(P<0.01).After interfering SNHG15, the results of Western blotting showed that the expression levels of EMT-related proteins Snail and CXCR4 decreased, the expression levels of Snail and CXCR4 increased in miRNA-451a inhibitor group(P<0.01), and the differences of the Vimentin expression level was not statistically significant(P>0.05).
      ConclusionsLncRNA SNHG15 may promote the migration and apoptosis of breast cancer cells by regulating miRNA-451a, and potentially regulate CXCR4 to induce EMT of breast cancer cells.

       

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