Exosome-transmitted miR-30a-5p enhances cell proliferation, migration, and invasion in ovarian cancer.

IF 2.8 4区 生物学 Q3 CELL BIOLOGY Cell Division Pub Date : 2023-11-01 DOI:10.1186/s13008-023-00099-2
Jian Cao, Huan Wang, Jing Yang, Jing Zhang, Dake Li, Pengfei Xu
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Abstract

Background: Ovarian cancer (OC) causes the highest rates of mortality among women's genital tract malignancies. Micro-ribonucleic acid (miRNA), the most abundant long noncoding RNAs transmitted by exosomes, has been revealed to be a potential marker for OC since 2008. In this study, we aimed to determine the possible roles of miRNAs derived from exosomes in the early diagnosis of OC through miRNA microarray, besides, exploring the underlying mechanisms of miRNAs in the OC progression.

Methods: We isolated exosomes from high invasive OC cell line HO8910PM and its parent cell line HO8910 using transmission electron microscopy and western blot, and performed miRNA microarray to identify the exosome-transmitted miRNA from the two cell lines, respectively. The expression profile was obtained by quantitative analysis, and then the differentially expressed individuals were screened. miRNA-30a-5p, a stable miRNA in both cells of our sequencing data was set for further study. MiR-30a-5p mimics, inhibitor and their corresponding negative controls were applied in OC cells. Then the cell proliferation, migration, and invasion of different groups were analyzed via cell counting-kit 8 (CCK8), wound healing, and Transwell analyses. Besides, ZBE2 and LDH2 expressions were detected by qRT-PCR.

Results: Combined with the data report of miRNA microarray technology, we set miR-30a-5p as our target miRNA to analyze its molecular function in regulating proliferation, migration, and invasion in OC cells. Our results showed that the miR-30a-5p overexpression could significantly enhance the capability of proliferation, migration, and invasion of HO8910 and HO8910PM cells, whereas the miR-30a-5p inhibition showed the opposite tendency (all P < 0.05). Besides, miR-30a-5p may be involved in these oncogenic processes through the upregulation of ZEB2 and LDH2.

Conclusion: Our results demonstrate that exosome-transmitted miRNA-30a-5p promotes the malignant behavior of OC cells, which may be served as a promising diagnostic and prognostic marker for patients with OC.

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外显子传递的miR-30a-5p增强了卵巢癌症的细胞增殖、迁移和侵袭。
背景:在女性生殖道恶性肿瘤中,卵巢癌症(OC)的死亡率最高。微小核糖核酸(miRNA)是由外泌体传递的最丰富的长非编码RNA,自2008年以来已被发现是OC的潜在标志物。在这项研究中,我们旨在通过miRNA微阵列来确定来源于外泌体的miRNA在OC早期诊断中的可能作用,此外,我们还探索了miRNA在OC进展中的潜在机制。方法:利用透射电子显微镜和蛋白质印迹技术从高侵袭性OC细胞系HO8910PM及其亲本细胞系HO8910中分离出外泌体,并进行miRNA微阵列,分别鉴定来自这两个细胞系的外泌体传递的miRNA。通过定量分析获得表达谱,然后筛选差异表达的个体。miRNA-30a-5p是我们测序数据中两个细胞中的一种稳定miRNA,用于进一步研究。在OC细胞中应用MiR-30a-5p模拟物、抑制剂及其相应的阴性对照。然后通过细胞计数试剂盒8(CCK8)、伤口愈合和Transwell分析来分析不同组的细胞增殖、迁移和侵袭。此外,通过qRT-PCR检测ZBE2和LDH2的表达。结果:结合miRNA微阵列技术的数据报告,我们将miR-30a-5p作为我们的靶miRNA,分析其在调节OC细胞增殖、迁移和侵袭中的分子功能。我们的结果表明,miR-30a-5p的过表达可以显著增强HO8910和HO8910PM细胞的增殖、迁移和侵袭能力,而miR-30a-5 P的抑制则表现出相反的趋势(均P 结论:我们的研究结果表明,外泌体传递的miRNA-30a-5p促进OC细胞的恶性行为,这可能是OC患者的一个有前途的诊断和预后标志物。
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来源期刊
Cell Division
Cell Division CELL BIOLOGY-
CiteScore
3.70
自引率
0.00%
发文量
5
审稿时长
>12 weeks
期刊介绍: Cell Division is an open access, peer-reviewed journal that encompasses all the molecular aspects of cell cycle control and cancer, cell growth, proliferation, survival, differentiation, signalling, gene transcription, protein synthesis, genome integrity, chromosome stability, centrosome duplication, DNA damage and DNA repair. Cell Division provides an online forum for the cell-cycle community that aims to publish articles on all exciting aspects of cell-cycle research and to bridge the gap between models of cell cycle regulation, development, and cancer biology. This forum is driven by specialized and timely research articles, reviews and commentaries focused on this fast moving field, providing an invaluable tool for cell-cycle biologists. Cell Division publishes articles in areas which includes, but not limited to: DNA replication, cell fate decisions, cell cycle & development Cell proliferation, mitosis, spindle assembly checkpoint, ubiquitin mediated degradation DNA damage & repair Apoptosis & cell death
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