ArticleBMC cancer2019
miR-632 promotes gastric cancer progression by accelerating angiogenesis in a TFF1-dependent manner.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- The association between miR-632 and major adverse cardiovascular and cerebrovascular events in patients with end-stage renal disease undergoing long-term hemodialysis.BMC nephrology · 2025Article
- A frog peptide provides new strategies for the intervention against skin wound healing.Cellular & molecular biology letters · 2023Article
- Article
- Establishment and Validation of a Ferroptosis-Related Long Non-Coding RNA Signature for Predicting the Prognosis of Stomach Adenocarcinoma.Frontiers in genetics · 2022Article
- Secretion of pro-angiogenic extracellular vesicles during hypoxia is dependent on the autophagy-related protein GABARAPL1.Journal of extracellular vesicles · 2021Article
- Regulation of angiogenesis by microRNAs in cancer.Molecular medicine reports · 2021Review
- Angiogenesis-related non-coding RNAs and gastrointestinal cancer.Molecular therapy oncolytics · 2021Review
- Current perspectives on the dysregulated microRNAs in gastric cancer.Molecular biology reports · 2020Review
- Zinc Finger Protein 521, Negatively Regulated by MicroRNA-204-5p, Promotes Proliferation, Motility and Invasion of Gastric Cancer Cells.Technology in cancer research & treatment · 2019Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundGastric cancer (GC) is a common malignant disease worldwide. Aberrant miRNAs expression contributes to malignant cells behaviour, and in preclinical research, miRNA targeting has shown potential for improving GC therapy. Our present study demonstrated that miR-632 promotes GC progression in a trefoil factor 1 (TFF1)-dependent manner.
methodsWe collected GC tissues and serum samples to detect miR-632 expression using real-time PCR. A dual-luciferase reporter assay was used to identify whether miR-632 directly regulates TFF1 expression. Tube formation and endothelial cell recruitment assays were performed with or without miR-632 treatment. Western blot and in situ hybridization assays were performed to detect angiogenesis and endothelial recruitment markers that are affected by miR-632.
resultsOur results showed that miR-632 is highly expressed in GC tissue and serum and negatively associated with TFF1 in GC. miR-632 improves tube formation and endothelial cell recruitment by negatively regulating TFF1 in GC cells. Recombinant TFF1 reversed miR-632-mediated angiogenesis. TFF1 is a target gene of miR-632.
conclusionsOur study demonstrated that miR-632 promotes GC progression by accelerating angiogenesis in a TFF1-dependent manner. Targeting of miR-632 may be a potential therapeutic approach for GC patients.
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