The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
| Autor: | Wei Liu, Guoying Cui, Junhui Liang, Yonghui Zou, Changzhong Li, Haomeng Zhang, Mingjun Fan, Mengqing Li, Feifei Niu, Tianyu Dai |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Carcinogenesis
Mice Nude Apoptosis Bioengineering Carcinoma Ovarian Epithelial Applied Microbiology and Biotechnology Mice akt/mtor signaling pathway Cell Movement In vivo lncrna tug1 Cell Line Tumor microRNA medicine Animals Humans Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Ovarian Neoplasms Gene knockdown Chemistry TOR Serine-Threonine Kinases General Medicine medicine.disease Gene Expression Regulation Neoplastic MicroRNAs ovarian cancer Cell culture mir-582-3p Cancer research Phosphorylation Female RNA Long Noncoding Ovarian cancer Proto-Oncogene Proteins c-akt TP248.13-248.65 Research Article Research Paper Signal Transduction Biotechnology |
| Zdroj: | Bioengineered, Vol 12, Iss 2, Pp 10771-10781 (2021) Bioengineered article-version (VoR) Version of Record |
| ISSN: | 2165-5987 2165-5979 |
| Popis: | Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p in vivo. Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend in vitro and in vivo. The novel miR-582-3p represses the malignant properties of OC via the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC. |
| Databáze: | OpenAIRE |
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