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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
Published on: April 13, 2015
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Telomere dysfunction suppresses multiple endocrine neoplasia in mice
Ji-Hyeon Lee1, Miriam Anver2, Maria Kost-Alimova3
1Diabetes, Endocrinology & Obesity Branch, National Institute of Diabetes & Digestive & Kidney Diseases, Bethesda, MD.
Genes & Cancer
|October 30, 2014
Summary
Telomerase plays a key role in multiple endocrine neoplasia (MEN) syndrome development. Inhibiting telomerase in a mouse model significantly reduced pituitary and pancreas tumors, suggesting telomerase as a therapeutic target for MEN.
Area of Science:
- Endocrinology
- Cancer Biology
- Genetics
Background:
- Multiple endocrine neoplasia (MEN) syndrome involves tumors in multiple endocrine tissues.
- The genetic basis of MEN is known, but tumorigenic mechanisms are unclear.
- The Cdk4 (R24C) mouse model exhibits pituitary and pancreatic tumors relevant to MEN.
Purpose of the Study:
- Investigate the role of telomerase in MEN pathogenesis.
- Determine if telomerase inhibition affects tumor development in the Cdk4 (R24C) mouse model.
Main Methods:
- Analyzed telomerase activity, telomere length, and aneuploidy in Cdk4 (R/R) cells.
- Generated Cdk4 (R24C) mice lacking the mTERC gene (mTERC (-/-) Cdk4 (R/R)).
- Assessed tumor development and progression in mTERC (-/-) Cdk4 (R/R) mice.
Main Results:
- Elevated telomerase activity and telomere length observed in Cdk4 (R/R) cells.
- mTERC (-/-) Cdk4 (R/R) cells showed reduced proliferation and transformation potential.
- mTERC (-/-) Cdk4 (R/R) mice exhibited significantly reduced pituitary and pancreatic tumorigenesis.
Conclusions:
- Telomerase is crucial for tumor development in the Cdk4 (R24C) mouse model of MEN.
- Telomere dysfunction suppresses tumor initiation and increases latency.
- Targeting telomerase may offer a therapeutic strategy for MEN-related tumors.
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