ArticleCell biology and toxicology2023
Hypermethylation of microRNA-497-3p contributes to progression of thyroid cancer through activation of PAK1/β-catenin.
Article in Cell biology and toxicology, 2023. 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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4 citing papers in PubMed, 6 citations in OpenAlex.
- Biologically Informed Machine Learning Prioritizes Dietary Supplements That Protect Neural Crest Cells from Ethanol-Induced Epigenetic Dysregulation and Developmental Impairment.International journal of molecular sciences · 2025Article
- LINC01214 Promotes Non-Small Cell Lung Cancer Through the miR-497-3p/HSP90AB1 Axis.Canadian respiratory journal · 2025Article
- MicroRNA-mediated epigenetic regulation of HDAC8 and HDAC6: Functional significance in cervical cancer.Non-coding RNA research · 2024Article
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9 authors at 1 institution in 1 country.
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Abstract
MicroRNA-497 (miR-497) has been reported to be a tumor-suppressive miRNA in thyroid cancer (TC), yet the mechanism is not clearly defined. In this study, we aim to determine the mechanism by which miR-497-3p affects the progression of TC. After characterization of low miR-497-3p expression pattern in TC and normal tissues, we assessed the correlation between miR-497-3p expression and clinicopathological features of TC patients. Its low expression shared associations with advanced tumor stage and lymph node metastasis. ChIP and methylation-specific PCR provided data showing that downregulation of miR-497-3p in TC tissues was induced by DNA methyltransferase-mediated hypermethylation. By performing dual-luciferase reporter assay, we identified that miR-497-3p targeted PAK1 while PAK1 could inhibit β-catenin expression. Through this mechanism, miR-497-3p exerted the anti-proliferative, anti-invasive, pro-apoptotic, and anti-tumorigenic effects on TC cells on the strength of the results from gain-of-function and rescue experiments. This study suggested that hypermethylation of miR-497-3p resulted in upregulation of β-catenin dependent on PAK1 and contributed to cancer progression in TC, which highlighted one of miR-mediated tumorigenic mechanism.
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