ArticleOpen medicine (Warsaw, Poland)2022
Overexpression of miR-100-5p inhibits papillary thyroid cancer progression via targeting FZD8.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 15 citations in OpenAlex.
- [Effects of miR-100-5p on proliferation and apoptosis of acute myeloid leukemia cells and the underlying molecular mechanism].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
- Role and potential mechanisms of miR‑100 in different diseases (Review).Oncology reports · 2025Review
- miR‑100: A key tumor suppressor regulatory factor in human malignant tumors (Review).International journal of molecular medicine · 2025Review
- Small extracellular vesicle miRNAs as biomarkers for predicting antitumor efficacy in lung adenocarcinoma treated with chemotherapy and checkpoint blockade.Frontiers in immunology · 2025Article
- Review
- Unleashing Wnts: Wnt Ligands Fuel Cancer Spread.Journal of cancer biology · 2025Article
- Frizzled receptors (FZDs) in Wnt signaling: potential therapeutic targets for human cancers.Acta pharmacologica Sinica · 2024Review
- Expression of miR-31-5p affects growth, migration and invasiveness of papillary thyroid cancer cells.Endocrine · 2023Article
- Review
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2 authors at 1 institution in 1 country.
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Abstract
Papillary thyroid cancer (PTC) is the most prevalent type of TC worldwide; however, its pathological process remains unclear at the molecular level. In the current study, we analyzed the microarray data of PTC tissues and non-neoplastic thyroid tissues, and confirmed miR-100-5p as a downregulated miRNA in PTC. Via bioinformatic approach, western blotting, and TOP/FOP-flash assay, miR-100-5p was observed to be involved in the inactivation of Wnt/β-catenin signaling in TPC-1 and KTC-1. Frizzled Class Receptor 8 (FZD8), the coupled receptor for canonical Wnt/β-catenin signaling, was verified to be targeted and inhibited by miR-100-5p in TPC-1 and KTC-1. In the function assay, miR-100-5p mimic repressed PTC cell proliferation and induced cell apoptosis of TPC-1 and KTC-1; meanwhile, transfection of full-length FZD8 attenuated the effect of miR-100-5p mimic. Moreover, in the collected samples, miR-100-5p was lowly expressed in PTC tissues compared with normal tissues, especially in those of advanced stage (Stage III/IV vs Stage I/II), while FZD8 was highly expressed in PTC tissues, which in PTC tissues was inversely correlated to miR-100-5p. Thus, we suggest that overexpression of miR-100-5p inhibits the development of PTC by targeting FZD8.
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