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Long Noncoding RNA CTC Inhibits Proliferation and Invasion by Targeting miR-146 to Regulate KIT in Papillary Thyroid
Baochun Liao1, Shi Liu2, Jiafeng Liu1
1Department of Thyroid Surgery, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China.
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.
Insights
Long non-coding RNA CTC inhibits papillary thyroid carcinoma (PTC) progression and chemoresistance by acting as a microRNA-146 decoy, targeting KIT. Downregulation of CTC and KIT, with increased miR-146, was observed in PTC tissues.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in various diseases, but their role in papillary thyroid carcinoma (PTC) remains underexplored.
- Understanding lncRNA functions is crucial for developing novel therapeutic strategies in oncology.
Purpose of the Study:
- To investigate the biological relevance and regulatory mechanisms of lncRNAs, specifically CTC, in papillary thyroid carcinoma (PTC).
- To elucidate the molecular pathway involving CTC, microRNA-146 (miR-146), and KIT in PTC progression and chemoresistance.
Main Methods:
- In vitro and in vivo assays were employed to assess the role of CTC in PTC cell migration and invasion.
- Mechanistic studies explored the interaction between CTC, miR-146, and KIT expression.
- Quantitative analysis of CTC, miR-146, and KIT levels in clinical PTC specimens compared to normal thyroid tissues.
Main Results:
- CTC was identified as a negative regulator of PTC cell migration and invasion.
- CTC functions as a miR-146 decoy, de-repressing KIT expression.
- Downregulation of CTC and KIT, coupled with elevated miR-146, was observed in PTC tissues, correlating with disease progression.
Conclusions:
- CTC acts as a competing endogenous RNA (ceRNA) to inhibit PTC progression and chemoresistance via the miR-146/KIT axis.
- CTC represents a potential therapeutic target for suppressing PTC progression.
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