microRNA-29c inhibits cell proliferation by targeting NASP in human gastric cancer.
microRNA-29c inhibits cell proliferation by targeting NASP in human gastric cancer.
复制标题
microRNA-29c 通过靶向 NASP 抑制人胃癌中的细胞增殖。
DOI：
10.1186/s12885-017-3096-9
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发表时间：
2017-02-07
期刊：
影响因子：
3.8
通讯作者：
Liu B
中科院分区：
文献类型：
--
作者：
Yu B;Chen X;Li J;Gu Q;Zhu Z;Li C;Su L;Liu B
胃癌是世界范围内最常见的恶性肿瘤之一。近年来的研究表明，microRNA在胃癌细胞增殖过程中起着重要的调控作用。microRNA-29 c（miR-29 c）在不同类型的肿瘤中起肿瘤抑制剂的作用。采用定量PCR方法检测67例胃癌组织和9株胃癌细胞系中miR-29 c的表达水平。采用细胞增殖实验、软琼脂集落形成实验、流式细胞术检测细胞凋亡和细胞周期变化，探讨miR-29 c对细胞增殖的影响。通过生物信息学算法预测目的基因，并通过双荧光素酶报告基因分析和Western blot分析进行验证。在这项研究中，我们证明了miR-29 c在胃癌组织和细胞系中下调。我们发现过表达miR-29 c可抑制细胞增殖，促进细胞凋亡，并使细胞周期阻滞于G1/G 0期。我们还表明，miR-29 c通过靶向核自身抗原精子蛋白（NASP）发挥这些作用。此外，NASP的缺失可以使由miR-29 c引起的表型变少。这些数据表明，miR-29 c抑制胃癌的增殖，并有可能作为早期生物标志物和新的治疗靶点。本文的在线版本（doi：10.1186/s12885-017-3096-9）包含补充材料，可供授权用户使用。
Gastric cancer is one of the most common malignancies worldwide. Recent studies have shown that microRNAs play crucial roles in regulating cellular proliferation process in gastric cancer. MicroRNA-29c (miR-29c) acts as a tumor suppressor in different kinds of tumors. Quantitative PCR was performed to evaluate miR-29c expression level in 67 patient gastric cancer tissues and 9 gastric cancer cell lines. The effects of miR-29c were explored by proliferation assay, soft agar colony formation assay, apoptosis and cell cycle analysis using flow cytometry. The target gene was predicted by bioinformatic algorithms and validated by dual luciferase reporter assay and Western blot analysis. In this study, we demonstrate that miR-29c is down-regulated in gastric cancer tissues and cell lines. We indicate that overexpression of miR-29c inhibits cell proliferation, promotes apoptosis and arrests cell cycle at G1/G0 phase. We additionally show that miR-29c exerts these effects by targeting Nuclear autoantigenic sperm protein (NASP). Moreover, depletion of NASP can elite the phenotypes caused by miR-29c. These data suggest that miR-29c inhibits proliferation in gastric cancer and could potentially serve as an early biomarker and a novel therapy target. The online version of this article (doi:10.1186/s12885-017-3096-9) contains supplementary material, which is available to authorized users.