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

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Listed:
  • 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
    Xiamen University
    Xiamen University)

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.

Suggested Citation

  • 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 & Guang-Hui Jin, 2020. "MEN1 deficiency leads to neuroendocrine differentiation of lung cancer and disrupts the DNA damage response," Nature Communications, Nature, vol. 11(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-14614-4
    DOI: 10.1038/s41467-020-14614-4
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