ArticleScientific reports2020
Long Noncoding RNA CTC Inhibits Proliferation and Invasion by Targeting miR-146 to Regulate KIT in Papillary Thyroid Carcinoma.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- A diagnostic signature derived from NK cell related genes in prostate cancer: insights from integrated scRNA-seq and bulk RNA-seq analyses with functional validation of KIT.Frontiers in immunology · 2026Article
- Epigenetic modulation of CTCs as a novel therapeutic target in oncology.Molecular and cellular biochemistry · 2026Review
- MicroRNA-mediated autophagy regulation in thyroid cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- LncRNA CASC9 facilitates papillary thyroid cancer development and doxorubicin resistance via miR-28-3p/BCL-2 axis and PI3K/AKT signaling pathway.Journal of cardiothoracic surgery · 2024Article
- Targeting the nucleic acid oxidative damage repair enzyme MTH1: a promising therapeutic option.Frontiers in cell and developmental biology · 2024Review
- miRNA in Molecular Diagnostics.Bioengineering (Basel, Switzerland) · 2022Review
- FOXP4-AS1 Inhibits Papillary Thyroid Carcinoma Proliferation and Migration Through the AKT Signaling Pathway.Frontiers in oncology · 2022Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several lines of evidence have shown that long non-coding RNAs (lncRNAs) are dysregulated in many diseases. Nevertheless, the biological relevance of the lncRNAs in papillary thyroid carcinoma (PTC) has not been fully explored. We demonstrated that CTC was a negative regulator of PTC cell migration and invasion in vitro and in vivo. We found that microRNA-146 (miR-146) is an inhibitory target of CTC. We then demonstrated that CTC functioned as a miR-146 decoy to de-repress expression of KIT. Further study demonstrated that CTC modulated the progression and chemoresistance of PTC cells via miR-146 and KIT. The analysis of hundreds of clinical specimens revealed that CTC and KIT levels were downregulated, whereas miR-146 levels were greater in PTC tissues than in normal thyroid. Their expression levels correlated with one another. In conclusion, CTC functions as a competing endogenous RNA to inhibit the progression and chemoresistance of PTC cells, and identifies CTC serve as a potential therapeutic agent to suppress PTC progression.
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Registered trials
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