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长链非编码 RNA MALAT1 通过靶向 miR-129-5p 促进三阴性乳腺癌的增殖和侵袭。

Long non-coding RNA MALAT1 promotes proliferation and invasion via targeting miR-129-5p in triple-negative breast cancer.

机构信息

Department of Breast and Thyroid Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000, China.

Department of Breast and Thyroid Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000, China.

出版信息

Biomed Pharmacother. 2017 Nov;95:922-928. doi: 10.1016/j.biopha.2017.09.005. Epub 2017 Sep 12.

Abstract

BACKGROUND

Long non-coding RNA Metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1) play important roles in tumor progression. In the present study, we determined the regulatory function of MALAT1 in triple-negative breast cancer (TNBC).

METHODS

A total of 43 cases of TNBC tissues and paired adjacent non-tumor tissues were collected for the research. MALAT1 expression was explored by qRT-PCR. In vitro functional validation experiments were used to determine the effect of MALAT1 on TNBC progression. We further identified the downstream target miRNAs for MALAT1.

RESULTS

Relative expression of MALAT1 was increased in TNBC tissues and cell lines. High MALAT1 expression was closely correlated to advance clinical features and poor overall survival in TNBC patients. Function assay showed that MALAT1 silencing significantly decreased cell proliferation, migration, and invasion. Flow cytometry assay revealed that MALAT1 inhibition significantly induced cell cycle arrest in the G0/G1 phase. In addition, we showed that the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p.

CONCLUSION

Our results demonstrated that the "MALAT1-miR-129-5p" axis might play an important role in the progression of TNBC, thereby might provide a potential therapeutic strategy for the treatment of TNBC.

摘要

背景

长链非编码 RNA 肺癌转移相关转录本 1(lncRNA MALAT1)在肿瘤进展中发挥重要作用。本研究旨在确定 MALAT1 在三阴性乳腺癌(TNBC)中的调控功能。

方法

收集了 43 例 TNBC 组织和配对的相邻非肿瘤组织进行研究。采用 qRT-PCR 检测 MALAT1 的表达。通过体外功能验证实验来确定 MALAT1 对 TNBC 进展的影响。进一步鉴定 MALAT1 的下游靶 miRNAs。

结果

MALAT1 在 TNBC 组织和细胞系中表达升高。MALAT1 高表达与 TNBC 患者的晚期临床特征和不良总生存期密切相关。功能测定表明,沉默 MALAT1 可显著降低细胞增殖、迁移和侵袭能力。流式细胞术分析显示,MALAT1 抑制可显著诱导细胞周期停滞在 G0/G1 期。此外,我们表明 MALAT1 对 TNBC 细胞进展的作用是由 miR-129-5p 介导的。

结论

我们的研究结果表明,“MALAT1-miR-129-5p”轴可能在 TNBC 的进展中发挥重要作用,从而为 TNBC 的治疗提供了一种潜在的治疗策略。

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