MEN1 deficiency leads to neuroendocrine differentiation of lung cancer and disrupts the DNA damage response

Huan Qiu, Bang-Ming Jin, Zhan-Feng Wang, Bin Xu, Qi-Fan Zheng, Li Zhang, Ling-Yu Zhu, Shuang Shi, Jun-Bo Yuan, Xiao Lin, Shu-Bin Gao and Guang-Hui Jin ()
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Huan Qiu: Xiamen University
Bang-Ming Jin: Xiamen University
Zhan-Feng Wang: China-Japan Union Hospital of Jilin University
Bin Xu: Xiamen University
Qi-Fan Zheng: Xiamen University
Li Zhang: Xiamen University
Ling-Yu Zhu: Xiamen University
Shuang Shi: Xiamen University
Jun-Bo Yuan: Xiamen University
Xiao Lin: Xiamen University
Shu-Bin Gao: Xiamen University
Guang-Hui Jin: Xiamen University

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract The MEN1 gene, a tumor suppressor gene that encodes the protein menin, is mutated at high frequencies in neuroendocrine (NE) tumors; however, the biological importance of this gene in NE-type lung cancer in vivo remains unclear. Here, we established an ATII-specific KrasG12D/+/Men1−/− driven genetically engineered mouse model and show that deficiency of menin results in the accumulation of DNA damage and antagonizes oncogenic Kras-induced senescence and the epithelial-to-mesenchymal transition during lung tumorigenesis. The loss of menin expression in certain human primary lung cancers correlates with elevated NE profiles and reduced overall survival.

Date: 2020
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DOI: 10.1038/s41467-020-14614-4

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