Silencing of the long noncoding RNA LINC01132 alleviates the oncogenicity of epithelial ovarian cancer by regulating the microRNA‑431‑5p/SOX9 axis
| Autor: | Xiangming Xiao, Wei Zhu, Jinqin Chen |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
ceRNA network
endocrine system diseases Carcinogenesis Cell miRNA sponge Mice Nude Apoptosis Biology Carcinoma Ovarian Epithelial Cell Movement Cell Line Tumor Sequence Homology Nucleic Acid microRNA Genetics medicine Gene silencing Animals Humans long noncoding RNA Aged Cell Proliferation Ovarian Neoplasms Mice Inbred BALB C Oncogene Base Sequence LINC01132 Competing endogenous RNA SOX9 Transcription Factor Articles General Medicine Cell cycle Middle Aged Molecular medicine Xenograft Model Antitumor Assays female genital diseases and pregnancy complications Long non-coding RNA Gene Expression Regulation Neoplastic MicroRNAs medicine.anatomical_structure Cancer research Female RNA Interference RNA Long Noncoding |
| Zdroj: | International Journal of Molecular Medicine |
| ISSN: | 1791-244X |
| Popis: | To date, the role of lncRNA long intergenic non-protein-coding RNA 1132 (LINC01132) expression in epithelial ovarian cancer (EOC) has not been explored. Thus, LINC01132 expression in EOC was assessed and the regulatory activity of LINC01132 on the malignant behaviours of EOC cells was investigated. Additionally, the molecular events that occurred downstream of LINC01132 in EOC cells were also revealed. In the present study, LINC01132 expression in EOC was verified by employing RT-qPCR. The effects of LINC01132 on the aggressive behaviours of EOC cells were revealed utilizing multiple functional experiments. The targeting interaction among LINC01132, microRNA-431-5p (miR-431-5p) and SRY-box 9 (SOX9) was demonstrated by RNA immunoprecipitation and luciferase reporter assay. Herein, LINC01132 was overexpressed in EOC and was significantly associated with poor patient prognosis. Functionally, cell experiments revealed that LINC01132 depletion produced cancer-suppressive effects in EOC cells and regulated cell proliferation, migration, invasion and apoptosis in vitro. Additionally, the loss of LINC01132 attenuated tumour growth in vivo. Mechanistically, LINC01132 acted as a competing endogenous RNA by sequestering miR-431-5p and consequently overexpressing SOX9 in EOC cells, forming a LINC01132/miR-431-5p/SOX9 axis. In rescue experiments, miR-431-5p inhibition or SOX9 reintroduction eliminated the anti-tumour effects of LINC01132 silencing on the pathological behaviours of EOC cells. Generally, LINC01132 exhibited oncogenic activities in EOC cells by regulating the outcome of the miR-431-5p/SOX9 axis, providing an effective target for EOC diagnosis, therapy and prognosis evaluation. |
| Databáze: | OpenAIRE |
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