Department of General Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Eur Rev Med Pharmacol Sci. 2019 Sep;23(18):7920-7928. doi: 10.26355/eurrev_201909_19006.
Gastric carcinoma (GC) is one common malignant tumor with high morbidity and mortality rates all over the world. Recently, numerous studies have showed that the microRNAs (miRNAs) dysregulation was implicated in GC carcinogenesis. This research aimed to explore the potential associations between miR-29c and cyclin-dependent kinase 6 (CDK6) in GC.
GC tissues and corresponding normal tissues were collected from 54 GC patients who underwent surgery at the Second Hospital of Anhui Medical University between 2015 and 2017. We measured the expressions of CDK6 and miR-29c in GC tissues using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). We next investigated the functions of miR-29c in GC cells by performing transwell assays. To further determine the correlation between miR-29c and CDK6 in GC cell invasion and migration, the rescue experiments were performed by co-transfecting miR-29c inhibitor and CDK6 siRNA into AGS cells.
MiR-29c expressions were significantly declined in GC tissues and cells. Additionally, functional assays showed that the miR-29c over-expression suppressed the invasion and migration capacities of GC cells. According to TargetScan and dual-luciferase reporter assays, CDK6 was identified as a new miR-29c target. Moreover, the knockout of CDK6 had similar effects as the miR-29c over-expression in GC cells. The current research indicated that miR-29c over-expression could inhibit tumor behaviors in GC partially via down-regulating CDK6.
We revealed that miR-29c down-regulated in GC tissues and cells. MiR-29c over-expression effectively suppressed the GC cell invasion and migration. Moreover, CDK6 was identified as a direct functional target of miR-29c in GC. The current study provides new insights for the GC treatment and suggests that miR-29c/CDK6 axis is a therapeutic candidate target for GC patients.
胃癌（GC）是一种常见的恶性肿瘤，发病率和死亡率均较高，遍及全球。最近，大量研究表明微小 RNA（miRNA）的失调与 GC 的发生发展有关。本研究旨在探讨 miR-29c 与细胞周期蛋白依赖性激酶 6（CDK6）在 GC 中的潜在关联。
收集 2015 年至 2017 年在安徽医科大学第二附属医院接受手术的 54 例 GC 患者的 GC 组织和相应的正常组织。采用实时定量聚合酶链反应（qRT-PCR）检测 GC 组织中 CDK6 和 miR-29c 的表达。通过 Transwell 实验研究 miR-29c 在 GC 细胞中的功能。为进一步确定 miR-29c 与 GC 细胞侵袭和迁移中的 CDK6 的相关性，通过将 miR-29c 抑制剂和 CDK6 siRNA 共转染入 AGS 细胞进行挽救实验。
miR-29c 在 GC 组织和细胞中的表达明显下调。此外，功能实验表明 miR-29c 的过表达抑制了 GC 细胞的侵袭和迁移能力。根据 TargetScan 和双荧光素酶报告基因实验，CDK6 被鉴定为 miR-29c 的一个新的靶基因。此外，CDK6 的敲除在 GC 细胞中与 miR-29c 的过表达具有相似的作用。本研究表明 miR-29c 过表达可能通过下调 CDK6 部分抑制 GC 肿瘤行为。
我们揭示了 miR-29c 在 GC 组织和细胞中下调。miR-29c 的过表达可有效抑制 GC 细胞的侵袭和迁移。此外，CDK6 被鉴定为 GC 中 miR-29c 的直接功能靶基因。本研究为 GC 的治疗提供了新的见解，并提示 miR-29c/CDK6 轴可能成为 GC 患者的治疗候选靶点。
