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周园红, 罗幼珍, 刘强, 刘晓雯. SNAI2基因对低转移潜能乳腺癌细胞恶性特征的影响及机制[J]. 肿瘤防治研究, 2018, 45(8): 528-532. DOI: 10.3971/j.issn.1000-8578.2018.17.1408
引用本文: 周园红, 罗幼珍, 刘强, 刘晓雯. SNAI2基因对低转移潜能乳腺癌细胞恶性特征的影响及机制[J]. 肿瘤防治研究, 2018, 45(8): 528-532. DOI: 10.3971/j.issn.1000-8578.2018.17.1408
ZHOU Yuanhong, LUO Youzhen, LIU Qiang, LIU Xiaowen. Effects and Regulatory Mechanisms of SNAI2 on Malignant Hallmarks of Non-Invasive Breast Tumor Cells[J]. Cancer Research on Prevention and Treatment, 2018, 45(8): 528-532. DOI: 10.3971/j.issn.1000-8578.2018.17.1408
Citation: ZHOU Yuanhong, LUO Youzhen, LIU Qiang, LIU Xiaowen. Effects and Regulatory Mechanisms of SNAI2 on Malignant Hallmarks of Non-Invasive Breast Tumor Cells[J]. Cancer Research on Prevention and Treatment, 2018, 45(8): 528-532. DOI: 10.3971/j.issn.1000-8578.2018.17.1408

SNAI2基因对低转移潜能乳腺癌细胞恶性特征的影响及机制

Effects and Regulatory Mechanisms of SNAI2 on Malignant Hallmarks of Non-Invasive Breast Tumor Cells

  • 摘要:
    目的 探讨SNAI2基因对低转移潜能乳腺癌MCF-7和T-47D细胞恶性特征的影响及潜在机制。
    方法 (1)采用慢病毒载体筛选SNAI2过表达的MCF-7和T-47D细胞;(2)采用MTT法检测细胞增殖能力,划痕实验检测细胞迁移能力,Hoechst 33342检查细胞抗凋亡能力;(3)Real-time PCR法检测细胞基因表达水平。
    结果 (1)经荧光显微镜观察证实SNAI2已成功转染入MCF-7和T-47D细胞中;(2)SNAI2的高表达能增强MCF-7和T-47D细胞的恶性特征,包括增殖、侵袭迁移及抗凋亡能力(P < 0.01);(3)SNAI2的高表达可促进MCF-7和T-47D细胞中Cyclin D1、MMP9和VIM的表达水平上调,E-CDH的表达水平下调(P < 0.01)。
    结论 SNAI2可通过促进低转移潜能乳腺癌细胞发生上皮细胞-间充质转化(EMT)获得更高的转移潜能,为进一步探索SNAI2在乳腺癌的基因靶向治疗提供新的方法和理论支撑。

     

    Abstract:
    Objective To explore the effects and related mechanisms of SNAI2 on malignant hallmarks of non-invasive breast tumor MCF-7 and T-47D cells.
    Methods (1) The lentiviral vector was used to screen MCF-7 and T-47D cells with SNAI2 overexpression; (2) The proliferation, migration and anti-apoptosis abilities of tumor cells were detected by MTT assay, wound healing and Hoechst 33342 assay, respectively; (3) The gene expression was tested by real-time PCR.
    Results (1) The GV367-SNAI2 was successfully transfected into MCF-7 and T-47D cells; (2)The SNAI2 could enhance malignant hallmarks of non-invasive breast tumor cells, including the proliferation, migration and anti-apoptosis abilities(P < 0.01); (3) The over-expression of SNAI2 could up-regulate the expression of Cyclin D1, MMP9, VIM and down-regulate the expression of E-CDH in MCF-7 and T-47D cells(P < 0.01).
    Conclusion SNAI2 could promote higher metastasis potential of non-invasive breast tumor cells through EMT, which will provide the experimental foundation for further exploring new targeted therapeutic method.

     

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