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首页> 外文期刊>RSC Advances >Long non-coding RNA NEAT1 contributes to docetaxel resistance of prostate cancer through inducing RET expression by sponging miR-34a
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Long non-coding RNA NEAT1 contributes to docetaxel resistance of prostate cancer through inducing RET expression by sponging miR-34a

机译：长非编码RNA NEAT1通过使miR-34a海绵化诱导RET表达，从而有助于前列腺癌的多西他赛耐药性

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Background: Nuclear paraspeckle assembly transcript 1 (NEAT1) was demonstrated to serve as a carcinogenic long non-coding RNA (lncRNA) in multiple tumors including prostate cancer (PC). However, the potential biological role of NEAT1 in docetaxel resistance of PC and the underlying mechanism are largely unknown. Methods: Expressions of NEAT1 and miR-34a in PC tissues and cells were detected by qRT-PCR. The IC50 value of docetaxel and apoptosis in PC cells were examined by CCK-8 assay and flow cytometry analysis, respectively. Bioinformatics software and a luciferase reporter assay were used to predict and confirm the potential targets of miR-34a. A tumor xenograft assay was employed to verify the effect of NEAT1 on docetaxel resistance of PC cells in vivo. Results: NEAT1 was upregulated and miR-34a was downregulated in PC tissues, parental PC cells and docetaxel-resistant PC cells. NEAT1 knockdown improved sensitivity to docetaxel in docetaxel-resistant PC cells. In addition, NEAT1 functioned as a ceRNA of miR-34a in docetaxel-resistant PC cells to positively regulate the expression of RET (rearranged during transfection). Moreover, miR-34a inhibition partially reversed NETA1-knockdown-induced sensitivity to docetaxel in docetaxel-resistant PC cells. NEAT1 overexpression partially overturned RET-knockdown-mediated sensitivity to docetaxel in docetaxel-resistant PC cells. Furthermore, NEAT knockdown enhanced docetaxel sensitivity of docetaxel-resistant PC cells in vivo. Conclusion: NEAT1 contributed to docetaxel resistance of PC through inducing RET expression by sponging miR-34a, implying that targeting the NEAT1/miR-34a/RET axis may be a potential application in improving chemotherapy of PC.
机译：背景：核副斑点装配转录本1（NEAT1）被证明在包括前列腺癌（PC）在内的多种肿瘤中起着致癌的长非编码RNA（lncRNA）的作用。但是，NEAT1在PC对多西他赛耐药中的潜在生物学作用及其潜在机制尚不清楚。 方法：用qRT-PCR检测NEAT1和miR-34a在PC组织和细胞中的表达。通过CCK-8法和流式细胞仪检测多西他赛的IC 50 值和PC细胞凋亡。使用生物信息学软件和荧光素酶报告基因测定法来预测和确认miR-34a的潜在靶标。肿瘤异种移植法用于验证NEAT1对体内 PC细胞多西他赛耐药的影响。 结果：PC组织，亲代PC细胞和多西他赛耐药PC细胞中NEAT1上调，而miR-34a下调。 NEAT1组合可提高耐多西他赛PC细胞对多西他赛的敏感性。此外，NEAT1在耐多西他赛的PC细胞中充当miR-34a的ceRNA，以正向调节RET的表达（在转染过程中重新排列）。此外，在抵抗多西他赛的PC细胞中，miR-34a的抑制作用部分逆转了NETA1-nockdown对多西他赛的敏感性。 NEAT1的过表达部分推翻了抗多西他赛的PC细胞中RET敲低介导的对多西他赛的敏感性。此外，NEAT敲除增强了耐多西他赛的PC细胞在体内的多西他赛敏感性。 结论：NEAT1通过刺激miR-34a诱导RET表达，从而促进PC对多西他赛的耐药性，这表明靶向NEAT1 / miR-34a / RET轴可能是改善PC化疗的潜在应用。

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