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目的探讨同源盒基因转录反义RNA(HOTAIR)调控乳腺癌细胞MDAMB-231转移的分子机制。方法以人乳腺癌细胞MDA-MB-231为研究材料,用小RNA干扰技术下调乳腺癌细胞HOTAIR表达,实时荧光定量聚合酶链反应检测HOTAIR下调水平。用细胞计数法检测HOTAI下调前后细胞增值能力变化,划痕实验(Wound Healing模型)检测下调HOTAIR前后乳腺癌细胞迁移能力变化。结果小干扰RNA下调HOTAIR表达后,乳腺癌MDA-MB-231细胞增殖能力显著降低(P<0.05);小干扰RNA下调HOTAIR表达后,siHOTAIR乳腺癌细胞的迁移能力显著下降。结论长链非编码RNA HOTAIR可促进乳腺癌MDA-MB-231细胞增殖迁移,可作为乳腺癌药物研制的潜在靶点。
OBJECTIVE: To investigate the molecular mechanism of homologous box gene transcriptional antisense RNA (HOTAIR) in regulating the metastasis of breast cancer cell line MDAMB-231. Methods Human breast cancer cell line MDA-MB-231 was used as a research material. The expression of HOTAIR in breast cancer cells was down-regulated by small RNA interference. The down-regulation of HOTAIR was detected by real-time fluorescence quantitative polymerase chain reaction. Cell viability was measured by cell counting before and after HOTAI down-regulation. Wound healing assay was used to detect the migration of HOTAIR cells. Results The proliferation of breast cancer MDA-MB-231 cells was significantly decreased after HOTAIR expression was down-regulated by small interfering RNA (P <0.05). The down-regulation of HOTAIR expression by siRNA decreased the migration ability of siHOTAIR breast cancer cells significantly. Conclusion Long-chain non-coding RNA HOTAIR can promote the proliferation and migration of breast cancer MDA-MB-231 cells, which may be used as a potential target for the development of breast cancer drugs.