Related Experiment Video
Updated: Jun 18, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Frequent epigenetic inactivation of RASSF10 in thyroid cancer
Undraga Schagdarsurengin1, Antje M Richter, Christina Wöhler
1Institute for Genetics, Justus-Liebig-University, Giessen, Germany.
Abstract:
The Ras association domain family (RASSF) encodes for distinct tumor suppressors and several members are frequently silenced in human cancer. In our study, we analyzed the role of a novel RASSF member termed RASSF10 in thyroid carcinogenesis. The RASSF10 CpG island promoter was intensively methylated in nine thyroid cancer cell lines and in 66% of primary thyroid carcinomas. RASSF10 methylation was significantly increased in primary thyroid carcinoma compared to normal thyroid and follicular adenoma (0 and 10%, respectively; p < 0.004). Patients with cancerous lymph nodes were significantly hypermethylated for RASSF10 in primary thyroid tumors compared to those with non-affected lymph nodes (79 vs. 36%; p = 0.047). RASSF10 promoter hypermethylation correlated with a reduced expression and treatment with a DNA methylation inhibitor reactivated RASSF10 transcription. In summary, our data show frequent epigenetic inactivation of RASSF10 in thyroid cancer. These results suggest that RASSF10 may encode a novel epigenetically inactivated candidate tumor suppressor gene in thyroid carcinogenesis.
Insights
Ras association domain family 10 (RASSF10) acts as a tumor suppressor. Frequent epigenetic silencing of RASSF10 was observed in thyroid cancer, suggesting its role in thyroid carcinogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- The Ras association domain family (RASSF) comprises tumor suppressor genes, with several members frequently silenced in human cancers.
- Epigenetic alterations, particularly DNA methylation, play a crucial role in cancer development.
Purpose of the Study:
- To investigate the role of a novel RASSF member, RASSF10, in thyroid carcinogenesis.
- To determine the frequency and significance of RASSF10 epigenetic inactivation in thyroid tumors.
Main Methods:
- Analysis of RASSF10 CpG island promoter methylation in thyroid cancer cell lines and primary tumors.
- Comparison of RASSF10 methylation levels between cancerous and non-cancerous thyroid tissues.
- Correlation of RASSF10 methylation with gene expression and lymph node status.
- Assessment of RASSF10 transcriptional reactivation upon DNA methylation inhibitor treatment.
Main Results:
- Intensive methylation of the RASSF10 promoter was found in nine thyroid cancer cell lines and 66% of primary thyroid carcinomas.
- RASSF10 methylation was significantly increased in primary thyroid carcinomas compared to normal thyroid and follicular adenoma (p < 0.004).
- Hypermethylation of RASSF10 was significantly associated with cancerous lymph nodes (79% vs. 36%, p = 0.047).
- RASSF10 promoter hypermethylation correlated with reduced gene expression, and DNA methylation inhibitor treatment reactivated RASSF10 transcription.
Conclusions:
- Frequent epigenetic inactivation of RASSF10 occurs in thyroid cancer.
- RASSF10 functions as a potential tumor suppressor gene epigenetically silenced during thyroid carcinogenesis.
- RASSF10 represents a novel candidate tumor suppressor gene in thyroid cancer development.
Related Concept Videos
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
The Ras Gene
Ras is a superfamily...
Abnormal Proliferation
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
