ArticleMolecular biotechnology2024
MiR-138-5p Inhibits Thyroid Cancer Cell Growth and Stemness by Targeting TRPC5/Wnt/β-Catenin Pathway.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- MicroRNAs in Esophageal Cancer: Implications for Diagnosis, Progression, Prognosis and Chemoresistance.International journal of molecular sciences · 2026Review
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- TRPC5 Promotes Intermittent Hypoxia-Induced Cardiomyocyte Injury Through Oxidative Stress.Nature and science of sleep · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs play a key role in the pathogenesis of many types of cancer, including thyroid cancer (TC). MiR-138-5p has been confirmed to be abnormally expressed in TC tissues. However, the role of miR-138-5p in TC progression and its potential molecular mechanism need to be further explored. In this study, quantitative real-time PCR was used to examine miR-138-5p and TRPC5 expression, and western blot analysis was performed to examine the protein levels of TRPC5, stemness-related markers, and Wnt pathway-related markers. Dual-luciferase reporter assay was used to assess the interaction between miR-138-5p and TRPC5. Cell proliferation, stemness, and apoptosis were examined using colony formation assay, sphere formation assay, and flow cytometry. Our data showed that miR-138-5p could target TRPC5 and its expression was negatively correlated with TRPC5 expression in TC tumor tissues. MiR-138-5p decreased proliferation, stemness, and promoted gemcitabine-induced apoptosis in TC cells, and this effect could be reversed by TRPC5 overexpression. Moreover, TRPC5 overexpression abolished the inhibitory effect of miR-138-5p on the activity of Wnt/β-catenin pathway. In conclusion, our data showed that miR-138-5p suppressed TC cell growth and stemness via the regulation of TRPC5/Wnt/β-catenin pathway, which provided some guidance for studying the potential function of miR-138-5p in TC progression.
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Registered trials
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