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Updated: Feb 7, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer
Published on: February 3, 2023
Long Non-coding Antisense RNA TNRC6C-AS1 Is Activated in Papillary Thyroid Cancer and Promotes Cancer Progression by
Dilidaer Muhanhali1, Tianyu Zhai1, Jingjing Jiang1
1Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China.
Abstract:
Context: Evidences have shown the important role of long non-coding antisense RNAs in regulating its cognate sense gene in cancer biology. Objective: Investigate the regulatory role of a long non-coding antisense RNA TNRC6C-AS1 on its sense partner TNRC6C, and their effects on the aggressiveness and iodine-uptake ability of papillary thyroid cancer (PTC). Design: TNRC6C-AS1 was identified as the target long non-coding RNA in PTC by using microarray analysis and computational analysis. In vitro gain/loss-of-function experiments were performed to investigate the effects of TNRC6C-AS1 and TNRC6C on proliferation, apoptosis, migration, invasion and iodine-uptake ability of TPC1 cells. Expression levels of TNRC6C-AS1 and TNRC6C of 30 cases of PTC tissues and its adjacent normal thyroid tissues were determined. Results: Downregulation of TNRC6C-AS1 or overexpression of TNRC6C inhibited proliferation, migration and invasion of TPC1 cells, while apoptosis and iodine uptake was promoted in TPC1 cells. Suppression of TNRC6C-AS1 significantly increased the expression of TNRC6C in TPC1 cells. The inhibitory effect of TNRC6C-AS1 knockdown on cell proliferation, migration and invasion was attenuated when the expression of TNRC6C was suppressed simultaneously, indicating TNRC6C is a functional target of TNRC6C-AS1. The expression of TNRC6C-AS1 was significantly higher, while the TNRC6C mRNA and protein were significantly lower in PTC tissues than normal adjacent tissues. There was a significant inverse correlation between TNRC6C-AS1 and TNRC6C mRNA in PTC tissue samples. Conclusions: TNRC6C-AS1 promotes the progression of PTC and inhibits its ability of iodine accumulation by suppressing the expression of TNRC6C. Targeting TNRC6C-AS1 - TNRC6C axis may be a new promising treatment for PTC.
Insights
Long non-coding RNA TNRC6C-AS1 promotes papillary thyroid cancer (PTC) progression by suppressing TNRC6C. Targeting this axis may offer new PTC treatment strategies.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Long non-coding antisense RNAs play crucial roles in regulating their cognate sense genes in cancer.
- Understanding these regulatory mechanisms is vital for developing targeted cancer therapies.
Purpose of the Study:
- To investigate the regulatory role of TNRC6C-AS1 on its sense partner TNRC6C.
- To determine the effects of this axis on papillary thyroid cancer (PTC) aggressiveness and iodine uptake.
Main Methods:
- Microarray and computational analysis identified TNRC6C-AS1 in PTC.
- In vitro gain/loss-of-function experiments assessed TNRC6C-AS1 and TNRC6C effects on TPC1 cells.
- Expression levels of TNRC6C-AS1 and TNRC6C were analyzed in PTC tissues and adjacent normal tissues.
Main Results:
- Downregulation of TNRC6C-AS1 or overexpression of TNRC6C inhibited PTC cell proliferation, migration, and invasion, while promoting apoptosis and iodine uptake.
- TNRC6C-AS1 knockdown increased TNRC6C expression, and this effect was dependent on TNRC6C.
- TNRC6C-AS1 was upregulated, and TNRC6C was downregulated in PTC tissues, showing an inverse correlation.
Conclusions:
- TNRC6C-AS1 promotes PTC progression and reduces iodine accumulation by suppressing TNRC6C.
- The TNRC6C-AS1-TNRC6C axis represents a potential therapeutic target for papillary thyroid cancer.
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