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宋鹏, 龙彤, 梁培育, 欧善际. 长链非编码RNA-MALAT1对前列腺癌细胞增殖及凋亡的影响[J]. 肿瘤防治研究, 2019, 46(5): 411-416. DOI: 10.3971/j.issn.1000-8578.2019.18.1198
引用本文: 宋鹏, 龙彤, 梁培育, 欧善际. 长链非编码RNA-MALAT1对前列腺癌细胞增殖及凋亡的影响[J]. 肿瘤防治研究, 2019, 46(5): 411-416. DOI: 10.3971/j.issn.1000-8578.2019.18.1198
SONG Peng, LONG Tong, LIANG Peiyu, OU Shanji. Effects of Long Non-coding RNA-MALAT1 on Proliferation and Apoptosis of Prostate Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2019, 46(5): 411-416. DOI: 10.3971/j.issn.1000-8578.2019.18.1198
Citation: SONG Peng, LONG Tong, LIANG Peiyu, OU Shanji. Effects of Long Non-coding RNA-MALAT1 on Proliferation and Apoptosis of Prostate Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2019, 46(5): 411-416. DOI: 10.3971/j.issn.1000-8578.2019.18.1198

长链非编码RNA-MALAT1对前列腺癌细胞增殖及凋亡的影响

Effects of Long Non-coding RNA-MALAT1 on Proliferation and Apoptosis of Prostate Cancer Cells

  • 摘要:
    目的 探讨长链非编码RNA-MALAT1对激素依赖性前列腺癌细胞增殖与凋亡的影响及其作用机制。
    方法 以激素依赖性前列腺癌细胞PC3和LNCaP为研究对象,对细胞进行MALAT1过表达及干扰处理,并通过MTT、流式细胞仪、基质胶和平板克隆等方法检测MALAT1过表达或干扰对细胞生物学行为的影响。Western blot检测MALAT1对与细胞周期及凋亡相关蛋白Cyclin D1、Bcl-2、Bax及p-ERK1/2表达的影响。
    结果 与对照组比较,MALAT1组细胞的增殖能力明显增强(P < 0.01),克隆形成能力、血管生成能力增强,G0/G1期细胞数量增多,凋亡率降低;si-MALAT1组细胞增殖能力明显低于对照组(P < 0.01),克隆形成能力、血管生成能力减弱,G0/G1期细胞数量减少,凋亡率升高。
    结论 MALAT1对前列腺癌的发生发展有促进作用,抑制MALAT1表达可能对前列腺癌的治疗具有重要意义。

     

    Abstract:
    Objective To investigate the effect of long non-coding RNA-MALAT1 on the proliferation and apoptosis of hormone-dependent prostate cancer cells and possible mechanisms.
    Methods MALAT1 overexpression and interference treatment were performed in the hormone-dependent prostate cancer PC3 and LNCaP cell lines. MTT assay, flow cytometry, Matrigel and clone formation were used to examine the effects of MALAT1 overexpression and interference on cell biological behavior. Western blot was used to evaluate the effects of MALAT1 on the expression of Cyclin D1, Bcl-2, Bax and p-ERK1/2.
    Results Compared with control group, MALAT1 group cells showed enhanced abilities of proliferation (P < 0.01), clone formation and angiogenesis; the cells number in the G0/G1 phase was increased; the apoptotic rate was decreased. In contrast, the cells in si-MALAT1 group showed significantly lower proliferation ability compared with control group (P < 0.01); the abilities of clone formation and angiogenesis were reduced; the number of cells in the G0/G1 phase was decreased, while apoptotic rate was increased.
    Conclusion MALAT1 promotes the occurrence and development of prostate cancer. The inhibition of MALAT1 expression may play important roles in the treatment of prostate cancer.

     

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