Menin molecular interactions: insights into normal functions and tumorigenesis
S K Agarwal1, P A Kennedy, P C Scacheri
1National Institute of Diabetes and Digestive and Kidney Diseases/NIH, 9000 Rockville Pike, Bethesda, MD 20892-1802, USA. SunitaA@intra.niddk.nih.gov
Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|July 8, 2005
Summary
Multiple endocrine neoplasia type 1 (MEN1) arises from mutations in the MEN1 gene. Loss of the menin protein disrupts its interaction with JunD, promoting tumor growth.
Area of Science:
- Genetics
- Molecular Biology
- Oncology
Background:
- Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder caused by germline mutations in the MEN1 tumor suppressor gene.
- Biallelic inactivation of the MEN1 gene, through mutation or loss of heterozygosity, is implicated in both hereditary and sporadic tumors.
- The MEN1 gene encodes the menin protein, a nuclear factor involved in various cellular processes.
Purpose of the Study:
- To investigate the role of the menin protein in tumor suppression.
- To elucidate the molecular mechanisms underlying menin's function in tumorigenesis.
Main Methods:
- Analysis of MEN1 gene mutations and protein expression in tumors.
- In vitro studies to identify menin-interacting proteins.
- Examination of menin's interaction with JunD and its effect on cell growth.
Main Results:
- Menin protein interacts with diverse cellular proteins, including transcription factors like JunD.
- Inactivation of menin alters its interaction with JunD, shifting its function from growth suppression to growth promotion.
- This switch in menin-JunD interaction provides a potential mechanism for MEN1-associated tumorigenesis.
Conclusions:
- The menin protein plays a critical role in tumor suppression through its interactions with other proteins.
- Dysregulation of the menin-JunD pathway is a key factor in the development of MEN1-related tumors.
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