ArticleFrontiers in cell and developmental biology2025
MiR-145-5p arrests the cell cycle by modulating SMAD5/cyclin D1 to inhibit gastric cancer progression.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- SNX8 regulates BMPR2-mediated SMAD5 proteostasis to drive epithelial-mesenchymal transition in hepatocellular carcinoma.Journal of translational medicine · 2026Article
- LncRNA OTUD6B-AS1 overexpression induces parthanatos in esophageal adenocarcinoma cells by binding to miR-145-5p and promoting AIF expression.American journal of translational research · 2026Article
- Shared molecular features and candidate pathways underlying gastric cancer-depression comorbidity: a systems biology analysis.Frontiers in bioinformatics · 2026Article
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11 authors.
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Abstract
Purpose: This study aimed to explore the dysregulation of miR-145-5p in gastric cancer (GC) and its effects on the proliferation and cell cycle of GC cells, exploring the potential regulatory mechanism of miR-145-5p in GC. Methods: In this study, the TCGA database combined with Microarray was used to detect differentially expressed microRNA (miRNA) in GC tissues and cells. Quantitative real-time (qRT)-PCR was used to further verify the expression of miR-145-5p in GC cells and the 41 pairs of GC tissues and adjacent tissues. A retrospective analysis was conducted on the correlation between miR-145-5p and the clinicopathological characteristics of patients with GC. The proliferation ability and cell cycle of AGS and MKN28 were detected by CCK-8, Edu and flow cytometry. The downstream target genes of miR-145-5p were screened by bioinformatics and further verified by the dual-luciferase reporter assay. Immunohistochemistry was used to detect the expression of SMAD5 in GC tissues. Western blot was used to detect cell cycle-related proteins that were regulated by siRNA SMAD5. Results: The expression of miR-145-5p was lower in GC tissues and cells compared with adjacent tissues and GES-1, and was related to the poor prognosis of patients with GC. Overexpression of miR-145-5p inhibited the proliferation of GC cells and blocked the cell cycle from G1 phase to S phase. MiR-145-5p targeted SMAD5 to inhibit the proliferation, and arrested the G1/S phase transition of GC cells. Mechanistically, SMAD5 siRNA significantly reduced CCND1 protein expression, Bioinformatics databases predicted that cyclin D1 was the transcription target gene of SMAD5. Moreover, the re-expression of cyclin D1 partially reversed the cell cycle arrest that was induced by SMAD5 depletion in GC cells. Conclusion: Taken together, these findings reveal a novel role of the miR-145-5p/SMAD5/cyclin D1 axis in modulating cell cycle progression and cell proliferation in GC, which may provide a prognostic biomarker for GC treatment.
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