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MicroRNA-363 inhibits ovarian cancer progression by inhibiting NOB1
Yang Lin1, Tianmin Xu1, Shunqing Zhou1
1Department of Obstetrics and Gynecology, The Second Hospital, Jilin University, Nanguan District, Changchun 130041, China.
Abstract:
In this study, we investigated the role of microRNA-363(miR-363) in ovarian cancer (OC) progression. MiR-363expression was downregulated in OC patient tissues and four OC cell lines (SKOV3, A2780, OVCAR and HO-8910). Low miR-363 levels were associated with advanced stage, lymph node metastasis, and poor prognosis in OC. MiR-363 overexpression decreased growth, colony formation, migration and invasiveness of SKOV3 cells. In addition, miR-363 overexpression in SKOV3 cells also decreased xenograft tumor size and weight in nude mice. Bioinformatics and dual luciferase reporter assays revealed that miR-363 suppresses expression of NIN1/RPN12 binding protein 1 homolog (NOB1) by binding to the 3'-UTR of its transcript. NOB1 expression inversely correlated with miR-363 levels in OC tissues. Thus miR-363 appears to play a tumor suppressor role in OC by inhibiting NOB1.
Insights
MicroRNA-363 (miR-363) acts as a tumor suppressor in ovarian cancer (OC). Lower miR-363 levels correlate with advanced OC stages and poor prognosis, while its restoration inhibits OC cell growth and metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ovarian cancer (OC) remains a leading cause of cancer-related deaths in women.
- Understanding the molecular mechanisms driving OC progression is crucial for developing effective therapies.
- MicroRNAs (miRNAs) are increasingly recognized for their roles in cancer development and progression.
Purpose of the Study:
- To investigate the role of microRNA-363 (miR-363) in ovarian cancer (OC) progression.
- To determine the molecular target and mechanism of action of miR-363 in OC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess miR-363 expression in OC tissues and cell lines.
- Cell proliferation, colony formation, migration, and invasion assays to evaluate the functional role of miR-363.
- In vivo xenograft tumor models in nude mice to assess the effect of miR-363 on tumor growth.
- Bioinformatics analysis and dual-luciferase reporter assays to identify and validate the direct target of miR-363.
Main Results:
- MiR-363 expression was significantly downregulated in OC patient tissues and OC cell lines.
- Low miR-363 levels were associated with advanced tumor stage, lymph node metastasis, and poorer patient prognosis.
- Overexpression of miR-363 inhibited OC cell proliferation, colony formation, migration, and invasion in vitro.
- MiR-363 overexpression reduced tumor growth and weight in vivo.
- NIN1/RPN12 binding protein 1 homolog (NOB1) was identified as a direct target of miR-363, with its expression inversely correlated to miR-363 levels in OC tissues.
Conclusions:
- MiR-363 functions as a tumor suppressor in ovarian cancer.
- MiR-363 inhibits OC progression by directly targeting and suppressing NOB1 expression.
- Restoring miR-363 levels may represent a potential therapeutic strategy for ovarian cancer.
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