ArticleOpen medicine (Warsaw, Poland)2022
miR-1273h-5p suppresses CXCL12 expression and inhibits gastric cancer cell invasion and metastasis.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Comprehensive analysis of prognosis and drug sensitivity of programmed cell death pattern-related genes in gastric cancer patients.Scientific reports · 2025Article
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- PVT1/miR-16/CCND1 axis regulates gastric cancer progression.Open medicine (Warsaw, Poland) · 2023Article
- Oral Microbiota and Tumor-A New Perspective of Tumor Pathogenesis.Microorganisms · 2022Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
The aim of this study was to verify the biological function of miR-1273h-5p in gastric cancer (GC) and its underlying mechanisms. The differential expression of microRNAs between GC and tumor-adjacent normal tissues was detected using microarrays, miR-1273h-5p, and chemokine (C-X-C motif) ligand 12 (CXCL12) mRNA, and protein levels were evaluated using polymerase chain reaction and Western blotting methods, cell proliferation, apoptosis, migration, and invasion were determined by CCK-8, flow cytometry, and transwell assay. Compared to tumor-adjacent normal tissue and gastric epithelial mucosa cell line cells, miR-1273h-5p was significantly downregulated in tissues and cells of GC. The overexpression of miR-1273h-5p could inhibit cell proliferation, migration, invasion, and promote cell apoptosis; in contrast, inhibition of miR-1273h-5p expression could reverse this process. Moreover, a significant upregulation of CXCL12 was observed when the miR-1273h-5p was downregulated in GC cells. Additionally, miR-1273h-5p significantly reduces tumor volume and weight. Thus, this study suggests that miR-1273h-5p regulates cell proliferation, migration, invasion, and apoptosis during GC progression by directly binding to CXCL12 mRNA 3'-untranslational regions, which may be a novel diagnostic and therapeutic target in GC.
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