ArticleCancer cell international2018
MiR-218 regulates epithelial-mesenchymal transition and angiogenesis in colorectal cancer via targeting CTGF.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Functional significance of miR-218 in lung cancer.Journal of cancer metastasis and treatment · 2026Article
- Inorganic Polyphosphate Triggers NLRP3 Inflammasome and Promotes the Epithelial-to-Mesenchymal Transition and Migration of Colorectal Cancer Cells Through TRPM8 Receptor.International journal of molecular sciences · 2025Article
- Exosomal long non-coding RNAs in gastrointestinal cancer: chemoresistance mediators and therapeutic targets.Journal of translational medicine · 2025Review
- miR-23b-3p Ameliorates LPS-Induced Pulmonary Fibrosis by Inhibiting EndMT via DPP4 Inhibition.Molecular biotechnology · 2025Article
- Article
- Role of STAT3 in cancer cell epithelial‑mesenchymal transition (Review).International journal of oncology · 2024Review
- Connective Tissue Growth Factor: Regulation, Diseases, and Drug Discovery.International journal of molecular sciences · 2024Review
- Anti-angiogenesis in colorectal cancer therapy.Cancer science · 2024Review
- Pien Tze Huang Inhibits Migration and Invasion of Hepatocellular Carcinoma Cells by Repressing PDGFRB/YAP/CCN2 Axis Activity.Chinese journal of integrative medicine · 2024Article
- Characterization of gastric cancer-stimulated signaling pathways and function of CTGF in cancer-associated fibroblasts.Cell communication and signaling : CCS · 2024Article
- Exosomal miR-218 derived from mesenchymal stem cells inhibits endothelial-to-mesenchymal transition by epigenetically modulating of BMP2 in pulmonary fibrosis.Cell biology and toxicology · 2023Article
- Mesenchymal stem cell-derived exosomes enriched with miR-218 reduce the epithelial-mesenchymal transition and angiogenesis in triple-negative breast cancer cells.European journal of medical research · 2023Article
- Cathepsin-facilitated invasion of BMI1-high hepatocellular carcinoma cells drives bile duct tumor thrombi formation.Nature communications · 2023Article
- Utilizing MiSeq Sequencing to Detect Circulating microRNAs in Plasma for Improved Lung Cancer Diagnosis.International journal of molecular sciences · 2023Article
- Article
- Article
- Multifunctional regulatory protein connective tissue growth factor (CTGF): A potential therapeutic target for diverse diseases.Acta pharmaceutica Sinica. B · 2022Review
- Differential Expression of miRNA-223 in Coronary In-Stent Restenosis.Journal of clinical medicine · 2022Article
- Micro-RNAs, the Cornerstones of the Future of Radiobiology in Head and Neck Cancers?Current oncology (Toronto, Ont.) · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelial-to-mesenchymal transition (EMT) and angiogenesis play important roles in colorectal cancer (CRC) development. Connective tissue growth factor (CTGF) has been reported to promote several kinds of cancer progression and miR-218 has been identified as a tumor suppressor miRNA. However, little is known about the function of miR-218 in CRC. Here we investigated the effects of miR-218 on EMT and angiogenesis process in CRC cells. As well, the relation between miR-218 and CTGF was identified. The mechanism of miR-218's function was illustrated.
methodsCRC cell lines were transfected with miR-218 mimics. Proliferation, migration and angiogenesis were identified by MTT assay, Transwell assay, colony formation assay and tube formation assay. Protein and mRNA expression levels of associated genes were measured by Western blotting and RT-PCR. Dual luciferase assay was used to determine the relation of miR-218 and CTGF.
resultsmiR-218 was down-regulated in CRC cell lines and over expression of miR-218 could significantly inhibit EMT and angiogenesis. CTGF was a direct target of miR-218. Up regulation of CTGF level after miR-218 transfection could sufficiently rescue the suppression effects on EMT and angiogenesis.
conclusionmiR-218 directly targets CTGF and inhibits its expression, leading to suppression on EMT and angiogenesis of CRC cells. miR-218 might be used as potential therapeutic strategy for CRC treatment.
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