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Published on: January 12, 2020
Promoting action of long non-coding RNA small nucleolar RNA host gene 4 in ovarian cancer
Chao Liu1, Shu Zhao2, Zhi Xiang Lv3
1Department of Obstetrics and Gynecology, Maternal and Child Health Hospital of Ningyang County, Tai'an City, Shandong Province, 271499, China.
Objective:
Long non-coding RNA (LncRNA) small nucleolar RNA host gene 4 (SNHG4) has been shown to be aberrantly expressed in a variety of cancers and involved in cancer development, but its role in ovarian cancer (OC) is unclear. The purpose of this study was to explore the biological function of SNHG4 in OC and reveal its potential downstream molecular targets.
Methods:
OC tumor tissue and normal tissue were collected; normal human ovarian epithelial cell line (IOSE80) and human ovarian cancer cell line (A2780, SKOV-3, OV-90 and CAOV3) were selected. RT-qPCR was used to detect SNHG4, miR-98-5p, and TMED5, while western blot was used to detect the protein expression levels of TMED5, Ki67, MMP-9, Bcl-2, Bax, Gsk3β, Wnt3a, and β-catenin. The subcellular localization of SNHG4 was assessed by nucleocytoplasmic separation assay. CCK-8, colony formation assay, flow cytometry, and Transwell were used to assess the biological behavior of OC cells. The targeting relationship between SNHG4, miR-98-5p and TMED5 was verified by dual luciferase reporter assay and RIP assay.
Results:
In OC, SNHG4 and TMED5 were highly expressed, and miR-98-5p was underexpressed. Knockdown of SNHG4 inhibited OC cell proliferation, migration and invasion, promoted apoptosis, and prevented Wnt/β-catenin pathway activation. The effect of knockdown of SNHG4 was reversed by knockdown of miR-98-5p or overexpression of TMED5. Mechanistically, SNHG4 competitively adsorbed miR-98-5p to mediate TMED5 expression, thereby activating the Wnt/β-catenin pathway.
Conclusion:
SNHG4 accelerates OC development via mediating the miR-98-5p/TMED5 axis and activating the Wnt/β-Catenin pathway. SNHG4 gene silencing might be a novel option for OC treatment.
Insights
Long non-coding RNA SNHG4 accelerates ovarian cancer (OC) development by regulating the miR-98-5p/TMED5 axis and Wnt/β-Catenin pathway. SNHG4 gene silencing shows potential as a novel OC treatment strategy.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Aberrant expression of long non-coding RNA (lncRNA) SNHG4 is implicated in various cancers.
- The specific role of SNHG4 in ovarian cancer (OC) progression remains largely undefined.
- Understanding SNHG4's function is crucial for developing targeted OC therapies.
Purpose of the Study:
- To investigate the biological function of SNHG4 in ovarian cancer (OC).
- To identify downstream molecular targets of SNHG4 in OC.
- To elucidate the mechanism underlying SNHG4-mediated OC development.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) and Western blot to assess gene and protein expression.
- Cell proliferation, migration, invasion, and apoptosis assays (CCK-8, colony formation, flow cytometry, Transwell).
- Dual luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
Main Results:
- SNHG4 and TMED5 were upregulated, while miR-98-5p was downregulated in OC tissues and cells.
- SNHG4 knockdown suppressed OC cell proliferation, migration, and invasion, induced apoptosis, and inhibited the Wnt/β-catenin pathway.
- SNHG4 acts as a molecular sponge for miR-98-5p, upregulating TMED5 and activating the Wnt/β-catenin pathway.
Conclusions:
- SNHG4 promotes OC development by modulating the miR-98-5p/TMED5 axis and activating the Wnt/β-catenin pathway.
- SNHG4 gene silencing represents a promising therapeutic strategy for ovarian cancer.
- Targeting the SNHG4/miR-98-5p/TMED5 axis offers a novel therapeutic avenue for OC.
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