miR-489 在胰腺癌增殖和凋亡中的作用

Maolan Zeng, Yanhua Zhou, Yinxia Zhang, Tiancheng Wang, Jing Wang
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摘要

目的:本研究旨在检测miR-489在胰腺癌(PC)组织和细胞中的表达,探讨miR-489对人PC细胞增殖和凋亡的影响,并揭示其潜在机制。方法:采用实时聚合酶链反应(qRT-PCR)定量评估miR-489在PC组织、PANC-1和HPDE6-C7细胞系中的表达。生物信息学的结合位点预测表明,AKT丝氨酸/苏氨酸激酶3(AKT3)可能是miR-489的潜在靶点。通过 qRT-PCR 检测了 AKT3 在 PC 组织和细胞中的表达,荧光素酶报告实验和 Western 印迹实验验证了靶基因的合理性。转染 miR-NC、miR-489 mimics 和 si-AKT3 后,用 MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide)测定法和流式细胞术检测了 miR-489 对 PANC-1 细胞增殖、细胞周期和细胞凋亡的生物学作用:结果:与正常邻近组织和正常胰腺细胞相比,miR-489 在 PC 组织和细胞中的表达明显下调。AKT3被认为是miR-489的下游基因,研究发现miR-489和AKT3的表达水平成反比,荧光素酶和Western印迹检测进一步证实了这一点。在随后的实验中,通过转染 miR-489 mimics 上调 miR-489 能显著抑制 PANC-1 细胞的增殖、阻断 G1/S 转换并诱导细胞凋亡。然而,过表达 AKT3 能明显抵消 miR-489 的生物效应:我们的研究结果表明,miR-489的上调可通过靶向AKT3抑制PC细胞增殖并促进细胞凋亡。
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Role of miR-489 in the proliferation and apoptosis of pancreatic carcinoma.

Purpose: The purpose of the present study was to detect the expression of miR-489 in pancreatic cancer (PC) tissues and cells, and to explore the effects of miR-489 on cell proliferation and apoptosis of human PC cells and to also uncover the underlying mechanism.

Methods: miR-489 expression was assessed by quantitative real time-polymerase chain reaction (qRT-PCR) in PC tissues and PANC-1 and HPDE6-C7 cell lines. The binding-site predictions by bioinformatics showed that AKT Serine/Threonine Kinase 3 (AKT3) might be a potential target of miR-489. AKT3 expression in PC tissues and cells was detected by qRT-PCR, luciferase report assay and Western blotting assay were used to verify the rationality of the target gene. The biological role of miR-489 on cell proliferation, cell cycle and apoptosis were determined in PANC-1 cells by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry after transfection with miR-NC, miR-489 mimics and si-AKT3.

Results: Compared with normal adjacent tissues and normal pancreatic cells, the expression of miR-489 was markedly down-regulated in PC tissues and cells. AKT3 was considered as a downstream gene of miR-489 and it was found that the expression levels of miR-489 and AKT3 were inversely proportional to each other, which was further confirmed by luciferase and Western blot assays. In subsequent experiments, up-regulation of miR-489 by transfection with miR-489 mimics significantly inhibited cell proliferation, blocked the G1/S transition and induced cell apoptosis of PANC-1 cells. However, overexpression of AKT3 significantly counteracted the biological effects of miR-489.

Conclusions: Our findings indicate that up-regulation of miR-489 could suppress PC cell proliferation and facilitate cell apoptosis through targeting AKT3. miR-489 and AKT3 might serve as potential targets in the therapy of PC.

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