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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-155 affects renal carcinoma cell proliferation, invasion and apoptosis through regulating GSK-3β/β-catenin
1Department of Urology Surgery, The First Central Hospital of Baoding, Baoding, Hebei, China. ruojingweirr@126.com.
Objective:
Glycogen Synthase Kinase-3β (GSK-3β) negatively regulates Wnt/β-catenin signaling pathway through degrading β-catenin protein. It plays an inhibitory role in various tumors, while the influence in the pathogenesis of renal carcinoma has not been elucidated. MicroRNA-155 (MiR-155) was found to be upregulated in renal carcinoma tissue. Bioinformatics analysis revealed the complementary binding site between miR-155 and 3'-UTR of GSK-3β. This study investigated the influence of miR-155 in regulating GSK-3β expression, Wnt/β-catenin signaling pathway activity, and renal carcinoma cell proliferation, invasion, and apoptosis.
Patients And Methods:
The targeted regulatory relationship between miR-155 and GSK-3β were tested by dual luciferase assay. Renal carcinoma tissue and benign renal tissue were collected to detect miR-155 and GSK-3β expressions. MiR-155, GSK-3β, and β-catenin levels were compared between HK-2 and 786-O cells. Renal carcinoma 786-O cells were cultured in vitro and divided into four groups, including miR-NC, anti-miR-155, pIRES2-blank, and pIRES2-GSK-3β groups. Cell apoptosis was evaluated by flow cytometry. Cell invasion was determined by transwell assay. Cell proliferation was assessed by EdU staining.
Results:
MiR-155 targeted regulated GSK-3β expression. MiR-155 and β-catenin expressions were significantly increased, while GSK-3β level was significantly declined in renal carcinoma tissue compared with benign renal tissue. MiR-155 and β-catenin expressions were significantly elevated, whereas GSK-3β level was significantly downregulated in 786-O cells compared with HK-2 cells. Anti-miR-155 or pIRES2-GSK-3β transfection significantly up-regulated GSK-3β expression, attenuated β-catenin level, restrained cell proliferation and invasion, and enhanced cell apoptosis.
Conclusions:
MiR-155 promoted renal carcinoma pathogenesis. Inhibition of miR-155 increased GSK-3β expression, attenuated Wnt/β-catenin signaling pathway, weakened proliferation and invasion, and facilitated apoptosis in renal carcinoma cells.
Insights
MicroRNA-155 (miR-155) promotes renal carcinoma by downregulating Glycogen Synthase Kinase-3β (GSK-3β) and activating the Wnt/β-catenin pathway. Inhibiting miR-155 reverses these effects, hindering cancer progression.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Glycogen Synthase Kinase-3β (GSK-3β) is a negative regulator of the Wnt/β-catenin signaling pathway, crucial in various cellular processes.
- GSK-3β's role in renal carcinoma pathogenesis is not fully understood, despite its inhibitory function in other cancers.
- MicroRNA-155 (miR-155) is frequently upregulated in renal carcinoma tissues.
Purpose of the Study:
- To investigate the regulatory relationship between miR-155 and GSK-3β in renal carcinoma.
- To determine the impact of miR-155 on the Wnt/β-catenin signaling pathway.
- To assess the effects of miR-155 on renal carcinoma cell proliferation, invasion, and apoptosis.
Main Methods:
- Dual luciferase assay to confirm the targeting of GSK-3β by miR-155.
- Analysis of miR-155, GSK-3β, and β-catenin expression in renal carcinoma and benign tissues, and in renal cell lines (HK-2 and 786-O).
- In vitro experiments using 786-O cells with miR-155 inhibition or GSK-3β overexpression to evaluate cell apoptosis, invasion, and proliferation.
Main Results:
- A direct regulatory relationship between miR-155 and GSK-3β was confirmed.
- Renal carcinoma tissues and cells exhibited significantly higher miR-155 and β-catenin levels, with concurrently lower GSK-3β levels compared to benign tissues/cells.
- Inhibition of miR-155 or overexpression of GSK-3β led to increased GSK-3β, decreased β-catenin, reduced proliferation and invasion, and enhanced apoptosis in renal carcinoma cells.
Conclusions:
- MiR-155 promotes the pathogenesis of renal carcinoma by targeting GSK-3β and activating the Wnt/β-catenin pathway.
- Inhibiting miR-155 represents a potential therapeutic strategy for renal carcinoma by restoring GSK-3β expression and suppressing tumor growth.
- The findings elucidate a novel mechanism by which miR-155 contributes to renal carcinoma development and progression.
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