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FGL2 promotes tumor progression in the CNS by suppressing CD103+ dendritic cell differentiation

Author

Listed:
  • Jun Yan

    (Capital Medical University
    Beijing Institute for Brain Disorders
    The University of Texas MD Anderson Cancer Center)

  • Qingnan Zhao

    (The University of Texas MD Anderson Cancer Center)

  • Konrad Gabrusiewicz

    (The University of Texas MD Anderson Cancer Center)

  • Ling-Yuan Kong

    (The University of Texas MD Anderson Cancer Center)

  • Xueqing Xia

    (The University of Texas MD Anderson Cancer Center)

  • Jian Wang

    (The University of Texas MD Anderson Cancer Center)

  • Martina Ott

    (The University of Texas MD Anderson Cancer Center)

  • Jingda Xu

    (The University of Texas MD Anderson Cancer Center)

  • R. Eric Davis

    (The University of Texas MD Anderson Cancer Center)

  • Longfei Huo

    (The University of Texas MD Anderson Cancer Center)

  • Ganesh Rao

    (The University of Texas MD Anderson Cancer Center)

  • Shao-Cong Sun

    (The University of Texas MD Anderson Cancer Center)

  • Stephanie S. Watowich

    (The University of Texas MD Anderson Cancer Center)

  • Amy B. Heimberger

    (The University of Texas MD Anderson Cancer Center)

  • Shulin Li

    (The University of Texas MD Anderson Cancer Center)

Abstract

Few studies implicate immunoregulatory gene expression in tumor cells in arbitrating brain tumor progression. Here we show that fibrinogen-like protein 2 (FGL2) is highly expressed in glioma stem cells and primary glioblastoma (GBM) cells. FGL2 knockout in tumor cells did not affect tumor-cell proliferation in vitro or tumor progression in immunodeficient mice but completely impaired GBM progression in immune-competent mice. This impairment was reversed in mice with a defect in dendritic cells (DCs) or CD103+ DC differentiation in the brain and in tumor-draining lymph nodes. The presence of FGL2 in tumor cells inhibited granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced CD103+ DC differentiation by suppressing NF-κB, STAT1/5, and p38 activation. These findings are relevant to GBM patients because a low level of FGL2 expression with concurrent high GM-CSF expression is associated with higher CD8B expression and longer survival. These data provide a rationale for therapeutic inhibition of FGL2 in brain tumors.

Suggested Citation

  • Jun Yan & Qingnan Zhao & Konrad Gabrusiewicz & Ling-Yuan Kong & Xueqing Xia & Jian Wang & Martina Ott & Jingda Xu & R. Eric Davis & Longfei Huo & Ganesh Rao & Shao-Cong Sun & Stephanie S. Watowich & A, 2019. "FGL2 promotes tumor progression in the CNS by suppressing CD103+ dendritic cell differentiation," Nature Communications, Nature, vol. 10(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-018-08271-x
    DOI: 10.1038/s41467-018-08271-x
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    Cited by:

    1. Qingnan Zhao & Jiemiao Hu & Lingyuan Kong & Shan Jiang & Xiangjun Tian & Jing Wang & Rintaro Hashizume & Zhiliang Jia & Natalie Wall Fowlkes & Jun Yan & Xueqing Xia & Sofia F. Yi & Long Hoang Dao & Da, 2023. "FGL2-targeting T cells exhibit antitumor effects on glioblastoma and recruit tumor-specific brain-resident memory T cells," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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