Menin signaling and therapeutic targeting in breast cancer.

Autor: Liu P; School of Life Sciences, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China., Shi C; School of Life Sciences, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China., Qiu L; School of Life Sciences, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China., Shang D; School of Life Sciences, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China., Lu Z; School of Life Sciences, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China., Tu Z; School of Life Sciences, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China., Liu H; School of Pharmacy, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China. Electronic address: hanqing@ujs.edu.cn.
Jazyk: angličtina
Zdroj: Current problems in cancer [Curr Probl Cancer] 2024 Aug; Vol. 51, pp. 101118. Date of Electronic Publication: 2024 Jul 04.
DOI: 10.1016/j.currproblcancer.2024.101118
Abstrakt: To date, mounting evidence have shown that patients with multiple endocrine neoplasia type 1 (MEN1) may face an increased risk for breast carcinogenesis. The product of the MEN1 gene, menin, was also indicated to be an important regulator in breast cancer signaling network. Menin directly interacts with MLL, EZH2, JunD, NF-κB, PPARγ, VDR, Smad3, β-catenin and ERα to modulate gene transcriptions leading to cell proliferation inhibition. Moreover, interaction of menin-FANCD2 contributes to the enhancement of BRCA1-mediated DNA repair mechanism. Ectopic expression of menin causes Bax-, Bak- and Caspase-8-dependent apoptosis. However, despite numbers of menin inhibitors were exploited in other cancers, data on the usage of menin inhibitors in breast cancer treatment remain limited. In this review, we focused on the menin associated signaling pathways and gene transcription regulations, with the aim of elucidating its molecular mechanisms and of guiding the development of novel menin targeted drugs in breast cancer therapy.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024. Published by Elsevier Inc.)
Databáze: MEDLINE
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