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目的探讨长链非编码ATB通过抑制miR-200c的表达促进乳腺癌细胞侵袭转移的作用及其机制。方法 q PCR检测不同乳腺癌细胞株中ATB和miR-200c的表达情况;双荧光素酶报告基因检测ATB与miR-200c的相互作用;MTT细胞增殖实验和Transwell侵袭实验检测沉抑制ATB后乳腺癌细胞增殖和侵袭能力的变化;MTT细胞增殖实验和Transwell侵袭实验检测抑制ATB后沉默miR-200c对乳腺癌细胞增殖和侵袭能力的逆转作用;Western blot检测抑制ATB后ZEB1和ZNF217蛋白的表达。结果与其他乳腺癌细胞相比,SKBr-3细胞株ATB表达水平最低,miR-200c的表达水平最高;ATB能与miR-200c的位点特异性结合,调控其表达活性;抑制ATB后可以增强乳腺癌细胞的增殖和侵袭能力,而沉默miR-200c后可以在一定程度上逆转ATB对乳腺癌细胞增殖和侵袭能力的影响;抑制ATB后ZEB1和ZNF217蛋白表达水平得到一定的恢复。结论 ATB在乳腺癌发生、发展过程中起重要作用,ATB可以靶向调节miR-200c调控乳腺癌细胞的增殖和侵袭能力。
Objective To investigate the role and mechanism of long-chain non-coding ATB in promoting the invasion and metastasis of breast cancer cells by inhibiting the expression of miR-200c. Methods qRT-PCR was used to detect the expression of ATB and miR-200c in different breast cancer cell lines. The dual luciferase reporter gene was used to detect the interaction between ATB and miR-200c. MTT cell proliferation assay and Transwell invasion assay were used to detect the expression of ATB and miR- Cell proliferation and invasiveness were examined by MTT assay and Transwell assay. The effect of silencing miR-200c on the proliferation and invasion of breast cancer cells was detected by Western blot. The expression of ZEB1 and ZNF217 protein was detected by Western blot. Results Compared with other breast cancer cells, SKBr-3 cells had the lowest level of ATB expression and the highest level of miR-200c expression. ATB could specifically bind to miR-200c and regulate its expression activity. Breast cancer cells proliferation and invasion ability, and silencing miR-200c can reverse the effect of ATB to a certain extent on the proliferation and invasion ability of breast cancer cells; The inhibition of ATB ZEB1 and ZNF217 protein expression levels to some recovery. Conclusion ATB plays an important role in the development and progression of breast cancer. ATB can regulate the proliferation and invasion ability of breast cancer cells regulated by miR-200c.