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Updated: Jul 27, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-138-5p Inhibits Thyroid Cancer Cell Growth and Stemness by Targeting TRPC5/Wnt/β-Catenin Pathway
Bo Huang1, YiChao Zhang1, Peng Sun1
1Department of General Surgery, The First Affiliated Hospital of Jinan University, No.613, Huangpu Street, Guangzhou, 510000, China.
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.
Insights
MicroRNA-138-5p suppresses thyroid cancer (TC) cell growth and stemness by targeting TRPC5. This microRNA inhibits proliferation and stemness, promoting apoptosis, and impacting the Wnt/β-catenin pathway in TC progression.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- MicroRNAs are crucial in cancer development, with miR-138-5p showing altered expression in thyroid cancer (TC).
- The precise role and molecular mechanisms of miR-138-5p in TC progression require further investigation.
Purpose of the Study:
- To elucidate the function of miR-138-5p in thyroid cancer (TC) progression.
- To investigate the molecular mechanism underlying miR-138-5p's role in TC, focusing on its interaction with TRPC5 and the Wnt/β-catenin pathway.
Main Methods:
- Quantitative real-time PCR and Western blot analysis to measure gene and protein expression.
- Dual-luciferase reporter assay to confirm the interaction between miR-138-5p and TRPC5.
- Cell-based assays (colony formation, sphere formation, flow cytometry) to assess proliferation, stemness, and apoptosis.
Main Results:
- miR-138-5p directly targets TRPC5, with inverse expression correlation in TC tissues.
- miR-138-5p inhibits TC cell proliferation and stemness, while enhancing gemcitabine-induced apoptosis.
- TRPC5 overexpression reverses the effects of miR-138-5p on cell behavior and Wnt/β-catenin pathway activity.
Conclusions:
- miR-138-5p acts as a tumor suppressor in thyroid cancer by inhibiting cell growth and stemness.
- The miR-138-5p/TRPC5/Wnt/β-catenin axis is a key regulatory pathway in TC progression.
- These findings offer insights into the potential therapeutic role of miR-138-5p in thyroid cancer treatment.
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