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microRNA-132 inhibits the proliferation, migration, and invasion of ovarian cancer cells by regulating CT10 oncogenic gene homolog II-related signaling pathways

BACKGROUND: Despite a large amount of evidence showing the involvement of microRNA-132 (miR-132) in the occurrence and prognosis of many different types of cancer, the role of miR-132 in ovarian cancer and its potential molecular mechanism have yet to be fully explained. METHOD: We studied the biolo...

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Detalles Bibliográficos
Autores principales: Jiang, Haiyan, Dai, Min, Wu, Yao, Dong, Yansong, Qi, Lei, Xi, Qinghua, Liang, Guiwen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798291/
https://www.ncbi.nlm.nih.gov/pubmed/35117808
http://dx.doi.org/10.21037/tcr-20-2435
Descripción
Sumario:BACKGROUND: Despite a large amount of evidence showing the involvement of microRNA-132 (miR-132) in the occurrence and prognosis of many different types of cancer, the role of miR-132 in ovarian cancer and its potential molecular mechanism have yet to be fully explained. METHOD: We studied the biological function and molecular mechanism of miR-132 in ovarian cancer cell lines and clinical tissue samples using quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blot, Luciferase reporter assay, CCK8 test, colony formation test, and scratch and Transwell assays. RESULTS: The expression level of miR-132 was significantly reduced in ovarian cancer cell lines and clinical tissue samples. When the level of miR-132 was increased, the proliferation, colony-forming, migration, and invasion abilities of ovarian cancer cells were significantly inhibited. We found that miR-132 inhibits the expression of transcription factor CT10 Oncogenic Gene Homologue II (CRKII) through specific targeting of mRNA 3'-UTR. We also observed a significant increase in CRKII expression in ovarian cancer. Notably, CRKII expression was negatively correlated with miR-132 expression in clinical ovarian cancer tissue. Down-regulation of CRKII had a similar inhibitory effect on miR-132 overexpression in ovarian cancer cells, while excessive expression of CRKII reversed the inhibitory effect mediated by the excessive expression of miR-132. CONCLUSIONS: miR-132 inhibits the proliferation, invasion, and migration abilities of ovarian cancer cells through targeting CRKII.