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miR-1182 通过靶向 hTERT 抑制卵巢癌细胞的转移和增殖。

MiR-1182 inhibited metastasis and proliferation of ovarian cancer by targeting hTERT.

机构信息

Department of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Mar;22(6):1622-1628. doi: 10.26355/eurrev_201803_14569.

DOI:10.26355/eurrev_201803_14569
PMID:29630105
Abstract

OBJECTIVE

To investigate the potential effect of miR-1182 on the development of ovarian cancer and the relevant mechanism.

PATIENTS AND METHODS

The expression levels of miR-1182 were detected in ovarian cancer tissues and cells (SKOV3) comparing with corresponding adjacent normal tissues and normal ovarian cell (IOSE80). Luciferase assay was performed to evaluate the interaction between miR-1182 and hTERT. The effects of the miR-1182/hTERT axis on SKOV3 cells were determined by subsequent experiments including cell proliferation, expression level of hTERT, the invasion and metastasis detection.

RESULTS

miR-1182 was found repressed in ovarian cancer tissues and we got the same results at the cellular level. In order to research potential target of miR-1182, we checked it in three publicly available algorithms, TargetScan, miRDB and microRNA. We found that hTERT is a direct target of miR-1182, and luciferase assays confirmed our hypothesis. The subsequent experiments showed that decreased expression of hTERT resulting from the up-regulation of miR-1182 could decelerate cell proliferation, invasion, and metastasis in ovarian cancer cells.

CONCLUSIONS

Our research discovers the suppressor function of miR-1182 in ovarian cancer by targeting hTERT, revealing that miR-1182/hTERT axis may be a potential therapeutic target for the treatment of ovarian cancer.

摘要

目的

研究 miR-1182 对卵巢癌发展的潜在影响及其相关机制。

患者与方法

检测卵巢癌组织和细胞(SKOV3)中 miR-1182 的表达水平,并与相应的相邻正常组织和正常卵巢细胞(IOSE80)进行比较。通过荧光素酶报告基因实验评估 miR-1182 与 hTERT 之间的相互作用。通过后续实验,包括细胞增殖、hTERT 表达水平、侵袭和转移检测,研究 miR-1182/hTERT 轴对 SKOV3 细胞的影响。

结果

miR-1182 在卵巢癌组织中表达下调,我们在细胞水平上也得到了相同的结果。为了研究 miR-1182 的潜在靶标,我们在三个公开可用的算法(TargetScan、miRDB 和 microRNA)中进行了检查。我们发现 hTERT 是 miR-1182 的直接靶标,荧光素酶报告基因实验证实了我们的假设。随后的实验表明,miR-1182 的上调导致 hTERT 表达降低,可减缓卵巢癌细胞的增殖、侵袭和转移。

结论

我们的研究通过靶向 hTERT 发现了 miR-1182 在卵巢癌中的抑制功能,表明 miR-1182/hTERT 轴可能是治疗卵巢癌的潜在治疗靶点。

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