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Retracted: MicroRNA‐31 weakens cisplatin resistance of medulloblastoma cells via NF‐κB and PI3K/AKT pathways
Author(s) -
Ma Hui,
Cao Wei,
Ding Meili
Publication year - 2020
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1616
Subject(s) - cisplatin , pi3k/akt/mtor pathway , viability assay , protein kinase b , transfection , apoptosis , cancer research , western blot , microrna , biology , cell growth , vimentin , microbiology and biotechnology , signal transduction , cell culture , immunology , gene , chemotherapy , biochemistry , genetics , immunohistochemistry
Abstract Background Medulloblastoma (MB) is a malignant intracranial tumor. Cisplatin is a broad‐spectrum antitumor drug. It is important to study the cisplatin resistance of MB cells for the treatment of MB. In this article, we preliminarily studied the cisplatin resistance of microRNA (miR)‐31 and the possible mechanism in DAOY and UW228 cells, laying a theoretical foundation for clinical treatment of MB. Methods Following anti‐miR‐31 and pre‐miR‐31 transfections, cell viability, BrdU, CyclinD1, and apoptosis levels of DAOY and UW228 cell were detected by CCK8, BrdU, and western blot. Meanwhile, migration, invasion, and western blot assay were respectively used to detect the functions of miR‐31 migration and invasion. miR‐31 levels were changed by cell transfection and detected by RT‐qPCR. Furthermore, the related‐proteins of pathways were also detected by western blot. Results Anti‐miR‐31 increased DAOY and UW228 cells viability, BrdU + numbers, and expression of CyclinD1. The migration/invasion rate and expression levels of MMP‐9 and vimentin after anti‐miR‐31 transfection were increased. Furthermore, anti‐miR‐31 enhanced cells' cisplatin resistance and triggered PI3K/AKT and NF‐κB pathways. Pre‐miR‐31 played opposite roles and promoted the apoptosis. Conclusion miR‐31 regulated cell growth, migration, invasion and cisplatin resistance of MB cells via PI3K/AKT and NF‐κB pathways.