miR-99a inhibits proliferation and migration of cervical cancer cells by targeting IGF1R.

Q2 Medicine Journal of Buon Pub Date : 2021-09-01
Li Han
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引用次数: 0

Abstract

Purpose: To explore the effects of miR-99a on the proliferation and migration of cervical cancer cells (CCCs) by targeting IGF1R.

Methods: miR-99a and IGF1R expression in C-33 A and C-4 II cells was interfered. Their effects on the proliferation, apoptosis, and migration of CCCs were analyzed by MTT assay, flow cytometry, and Transwell assay. The mechanism of action of miR-99a was analyzed by a rescue experiment and a dual luciferase reporter gene assay (DLRGA). Differences in miR-99a and IGF1R expression were detected in cervical cancer and adjacent tissues (n=30 each), and the correlation of the expression with clinicopathological characteristics of patients with cervical cancer was analyzed.

Results: miR-99a expression was lower but IGF1R expression was higher in C-33 A and C-4 II cells than that in normal cervical epithelial cells. The results showed that both the promotion and the inhibition significantly decreased the proliferation and migration of the two CCCs, but increased their apoptosis. To further verify the correlation of miR-99a with IGF1R in cervical cancer, we co-transfected miR-99a and IGF1R overexpression vectors into the cells and found that compared with CCCs transfected with miR-99a overexpression vectors alone, the expression of IGF1R in the co-transfection group increased, while the expression of miR-99a did not change significantly. Additionally, the proliferation and migration of the cells in the co-transfection group increased, while their apoptotic rate decreased. DLRGA showed the targeted inhibition of miR-99a on IGF1R expression.

Conclusions: miR-99a can specifically inhibit IGF1R expression and thus inhibit the proliferation and migration of CCCs.

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miR-99a通过靶向IGF1R抑制宫颈癌细胞的增殖和迁移。
目的:探讨miR-99a靶向IGF1R对宫颈癌细胞(CCCs)增殖和迁移的影响。方法:干扰C-33 A和C-4 II细胞中miR-99a和IGF1R的表达。采用MTT法、流式细胞术和Transwell法分析其对CCCs增殖、凋亡和迁移的影响。通过救援实验和双荧光素酶报告基因测定(DLRGA)分析miR-99a的作用机制。检测miR-99a和IGF1R在宫颈癌及癌旁组织中的表达差异(各30例),并分析其表达与宫颈癌患者临床病理特征的相关性。结果:C-33 A和C-4 II细胞中miR-99a表达低于正常宫颈上皮细胞,而IGF1R表达高于正常宫颈上皮细胞。结果表明,促进和抑制均能显著降低两种CCCs的增殖和迁移,但增加其凋亡。为了进一步验证miR-99a与IGF1R在宫颈癌中的相关性,我们将miR-99a和IGF1R过表达载体共转染到细胞中,发现与单独转染miR-99a过表达载体的CCCs相比,共转染组IGF1R的表达增加,而miR-99a的表达没有明显变化。此外,共转染组细胞的增殖和迁移能力增强,细胞凋亡率降低。DLRGA显示miR-99a对IGF1R表达的靶向抑制。结论:miR-99a可以特异性抑制IGF1R的表达,从而抑制CCCs的增殖和迁移。
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来源期刊
Journal of Buon
Journal of Buon 医学-肿瘤学
自引率
0.00%
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0
审稿时长
4-8 weeks
期刊介绍: JBUON aims at the rapid diffusion of scientific knowledge in Oncology. Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board. With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world. With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers. JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.
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