MicroRNA-17-5p induces drug resistance and invasion of ovarian carcinoma cells by targeting PTEN signaling.

IF 1.9 3区 生物学 Q2 BIOLOGY Journal of Biological Research-Thessaloniki Pub Date : 2015-10-22 eCollection Date: 2015-12-01 DOI:10.1186/s40709-015-0035-2
Ying Fang, Changyan Xu, Yan Fu
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引用次数: 2

Abstract

Background: The miR-17-5p was overexpressed in ovarian cancer cells, and those cells were treated with paclitaxel. The proliferation of ovarian cancer cells was assessed by MTT assay. The Caspase-Glo3/7 and TUNEL assay were used to examine the effect of miR-17-5p on paclitaxel-induced apoptosis in ovarian cancer cells. The migration and invasion of ovarian cancer cells were analyzed by BD matrigel assays. Western blot was performed to evaluate the expression of apoptotic proteins and epithelial-mesenchymal transition markers in ovarian cancer cells.

Results: The survival rate of ovarian cancer cells was increased after overexpression of miR-17-5p. The apoptosis decreased in miR-17-5p overexpressed ovarian cancer cells. Altered miR-17-5p expression affected migration and invasion of ovarian cancer cells. The overexpression of miR-17-5p altered the expression of EMT markers. miR-17-5p activates AKT by downregulation of PTEN in ovarian cancer cells.

Conclusion: Our results indicate that miR-17-5p might serve as potential molecular therapeutic target.

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MicroRNA-17-5p通过靶向PTEN信号诱导卵巢癌细胞耐药和侵袭。
背景:miR-17-5p在卵巢癌细胞中过表达,这些细胞用紫杉醇处理。MTT法测定卵巢癌细胞增殖情况。采用Caspase-Glo3/7和TUNEL检测miR-17-5p对紫杉醇诱导的卵巢癌细胞凋亡的影响。采用BD矩阵法分析卵巢癌细胞的迁移和侵袭。Western blot检测卵巢癌细胞中凋亡蛋白和上皮间质转化标志物的表达。结果:过表达miR-17-5p后,卵巢癌细胞存活率提高。miR-17-5p过表达的卵巢癌细胞凋亡减少。miR-17-5p表达改变影响卵巢癌细胞的迁移和侵袭。过表达miR-17-5p改变EMT标志物的表达。miR-17-5p在卵巢癌细胞中通过下调PTEN激活AKT。结论:我们的研究结果表明miR-17-5p可能是潜在的分子治疗靶点。
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来源期刊
CiteScore
5.20
自引率
0.00%
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审稿时长
>12 weeks
期刊介绍: Journal of Biological Research-Thessaloniki is a peer-reviewed, open access, international journal that publishes articles providing novel insights into the major fields of biology. Topics covered in Journal of Biological Research-Thessaloniki include, but are not limited to: molecular biology, cytology, genetics, evolutionary biology, morphology, development and differentiation, taxonomy, bioinformatics, physiology, marine biology, behaviour, ecology and conservation.
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