Journal
BIOENGINEERED
Volume 12, Issue 2, Pages 10771-10781Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2021.2003662
Keywords
miR-582-3p; ovarian cancer; lncRNA TUG1; AKT; mTOR signaling pathway
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The study found that miRNA miR-582-3p is downregulated in ovarian cancer, and knockdown of miR-582-3p promotes proliferation and migration of OC cells while overexpression inhibits their development. Long non-coding RNA TUG1 binds to miR-582-3p and plays a negative regulatory role in the progression of OC. The AKT/mTOR signaling pathway suppresses the malignant properties of OC through targeting lncRNA TUG1.
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.
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