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微小RNA-211通过靶向富含半胱氨酸的酸性分泌蛋白抑制宫颈癌的增殖、侵袭和迁移。

miR-211 inhibits proliferation, invasion and migration of cervical cancer via targeting SPARC.

作者信息

Qu Xuqin, Gao Dezhen, Ren Qingxia, Jiang Xiufang, Bai Jianhua, Sheng Li

机构信息

Reproductive Center, Yantaishan Hospital, Yantai, Shandong 264001, P.R. China.

Department of Blood Transfusion, Yuhuangding Hospital, Yantai, Shandong 264000, P.R. China.

出版信息

Oncol Lett. 2018 Jul;16(1):853-860. doi: 10.3892/ol.2018.8735. Epub 2018 May 17.

Abstract

Cervical cancer remains one of the most frequent gynecological malignancies among females around the world. Therefore, fully understanding the molecular mechanisms underlying the progression of cervical cancer may be critical for the development of effective therapeutic strategies against cervical cancer. The object was to evaluate the potential effect of miR-211 and verify its influence on the function of secreted protein acidic and rich in cysteine (SPARC) in cervical cancer. It was demonstrated that miR-211 was downregulated in cervical cancer cell lines (HeLa and C33A) and cervical cancer specimens, while SPARC expression level was higher in tumor tissues. We also revealed miR-211 upregulated expression could inhibit cells proliferation, migration and invasion . SPARC was confirmed as a direct and functional target of miR-211 and the inverse relationship between them was also observed. The results of the present study suggest that miR-211 reduced cancer growth, migration and invasion, and suppresses the SPARC expression in cervical cancer. This newly identified miR-211 may provide further insight into the progression and offers a promising target for cervical cancer therapy.

摘要

宫颈癌仍然是全球女性中最常见的妇科恶性肿瘤之一。因此,全面了解宫颈癌进展的分子机制对于开发有效的宫颈癌治疗策略可能至关重要。目的是评估miR-211的潜在作用,并验证其对宫颈癌中富含半胱氨酸的酸性分泌蛋白(SPARC)功能的影响。结果表明,miR-211在宫颈癌细胞系(HeLa和C33A)和宫颈癌标本中表达下调,而SPARC在肿瘤组织中的表达水平较高。我们还发现miR-211表达上调可抑制细胞增殖、迁移和侵袭。SPARC被证实是miR-211的直接功能性靶点,并且观察到它们之间呈负相关。本研究结果表明,miR-211可降低宫颈癌的生长、迁移和侵袭,并抑制SPARC的表达。这种新发现的miR-211可能为宫颈癌的进展提供进一步的见解,并为宫颈癌治疗提供一个有前景的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f0c/6019960/ebc5a261c1be/ol-16-01-0853-g00.jpg

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