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Menin in Cancer

Overview
Journal Genes (Basel)
Publisher MDPI
Date 2024 Sep 28
PMID 39336822
Authors
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Abstract

The protein menin is encoded by the gene and primarily serves as a nuclear scaffold protein, regulating gene expression through its interaction with and regulation of chromatin modifiers and transcription factors. While the scope of menin's functions continues to expand, one area of growing investigation is the role of menin in cancer. Menin is increasingly recognized for its dual function as either a tumor suppressor or a tumor promoter in a highly tumor-dependent and context-specific manner. While menin serves as a suppressor of neuroendocrine tumor growth, as seen in the cancer risk syndrome multiple endocrine neoplasia type 1 (MEN1) syndrome caused by pathogenic germline variants in , recent data demonstrate that menin also suppresses cholangiocarcinoma, pancreatic ductal adenocarcinoma, gastric adenocarcinoma, lung adenocarcinoma, and melanoma. On the other hand, menin can also serve as a tumor promoter in leukemia, colorectal cancer, ovarian and endometrial cancers, Ewing sarcoma, and gliomas. Moreover, menin can either suppress or promote tumorigenesis in the breast and prostate depending on hormone receptor status and may also have mixed roles in hepatocellular carcinoma. Here, we review the rapidly expanding literature on the role and function of menin across a broad array of different cancer types, outlining tumor-specific differences in menin's function and mechanism of action, as well as identifying its therapeutic potential and highlighting areas for future investigation.

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References
1.
Lin W, Francis J, Li H, Gao X, Pedamallu C, Ernst P . Kmt2a cooperates with menin to suppress tumorigenesis in mouse pancreatic islets. Cancer Biol Ther. 2016; 17(12):1274-1281. PMC: 5199165. DOI: 10.1080/15384047.2016.1250986. View

2.
Wolffhardt T, Ketzer F, Telese S, Wirth T, Ushmorov A . Dependency of B-Cell Acute Lymphoblastic Leukemia and Multiple Myeloma Cell Lines on MEN1 Extends beyond MEN1-KMT2A Interaction. Int J Mol Sci. 2023; 24(22). PMC: 10670986. DOI: 10.3390/ijms242216472. View

3.
Olsen S, Godfrey L, Healy J, Choi Y, Kai Y, Hatton C . MLL::AF9 degradation induces rapid changes in transcriptional elongation and subsequent loss of an active chromatin landscape. Mol Cell. 2022; 82(6):1140-1155.e11. PMC: 9044330. DOI: 10.1016/j.molcel.2022.02.013. View

4.
Timar J, Kashofer K . Molecular epidemiology and diagnostics of KRAS mutations in human cancer. Cancer Metastasis Rev. 2020; 39(4):1029-1038. PMC: 7680318. DOI: 10.1007/s10555-020-09915-5. View

5.
Kulkoyluoglu-Cotul E, Arca A, Madak-Erdogan Z . Crosstalk between Estrogen Signaling and Breast Cancer Metabolism. Trends Endocrinol Metab. 2018; 30(1):25-38. DOI: 10.1016/j.tem.2018.10.006. View