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首页> 外文期刊>Journal of cellular physiology. >miR-483-3p suppresses the proliferation and progression of human triple negative breast cancer cells by targeting the HDAC8 oncogene
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miR-483-3p suppresses the proliferation and progression of human triple negative breast cancer cells by targeting the HDAC8 oncogene

机译：mir - 483 - 3 - p抑制增殖和人类三阴性乳腺癌的进展肿瘤细胞通过瞄准HDAC8致癌基因

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摘要

Triple negative breast cancer (TNBC) is a heterogeneous subclass of breast cancer (BC) distinguished by lack of hormone receptor expression. It is highly aggressive and difficult to treat with traditional chemotherapeutic regimens. Targeted-therapy using microRNAs (miR) has recently been proposed to improve the treatment of TNBC in the early stages. Here, we explore the roles of miR-483-3p/HDAC8 HDAC8 premiR-vector on tumorigenicity in TNBC patients. Clinical TNBC specimens and three BC cell lines were prepared. miR-483-3p and expression levels were measured using quantitative real-time polymerase chain reaction. Cell cycle progression was assessed by a flow-cytometry method. We also investigated cell proliferation by 3-2, 5-diphenyl tetrazolium bromide assay and colony formation assay. We used a to overexpress miR-483-3p, and a HDAC8-KO-vector for knocking out the endogenous production of HDAC8. Our data showed significant downregulation of miR-483-3p expression in TNBC clinical and cell line samples. The HDAC8 was also upregulated in both tissue specimens and BC cell lines. We found that increased levels of endogenous miR-483-3p affects tumorigenecity of MDA-MB-231. Downregulation of HDAC8 using the KO-vector showed the same pattern. Our results revealed that the miR-483-3p suppresses cellular proliferation and progression in TNBC cell lines via targeting HDAC8. Overall, our outcomes demonstrated the role of miR-483-3p as a tumor suppressor in TNBC and showed the possible mechanism via HDAC8. In addition, targeted treatment of TNBC with miR-483-3p might be considered in the future.
机译：三阴乳腺癌(TNBC)异构的子类乳腺癌(BC)区分缺乏激素受体表达式。与传统化疗治疗方案。最近提出的改善治疗TNBC的早期阶段。探索的角色mir - 483 - 3 - p / HDAC8 HDAC8premiR-vector TNBC患者的致瘤性。临床TNBC标本和公元前三个细胞株都准备好了。使用定量实时测量聚合酶链反应。评估了流式细胞术方法。调查由3 - 2细胞增殖,5-diphenyl溴化四唑试验和殖民地分析形成。mir - 483 - 3 - p,和HDAC8-KO-vector敲门从内生HDAC8的生产。显示的差别明显对这些mir - 483 - 3 - p表达TNBC临床和细胞系样本。组织标本和BC细胞系。水平的提高内源性mir - 483 - 3 - p的影响tumorigenecity mda - mb - 231。使用KO-vector HDAC8显示相同的模式。抑制细胞增殖和进展通过针对HDAC8 TNBC的细胞系。我们的结果证明了mir - 483 - 3 - p的角色作为一个肿瘤抑制TNBC和显示通过HDAC8可能机制。靶向治疗的TNBC mir - 483 - 3 - p被认为是在未来。

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