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GALNT14 promotes lung-specific breast cancer metastasis by modulating self-renewal and interaction with the lung microenvironment

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  • Ki-Hoon Song

    (Korea Advanced Institute of Science and Technology (KAIST))

  • Mi So Park

    (Korea Advanced Institute of Science and Technology (KAIST))

  • Tulip S. Nandu

    (University of Texas Southwestern Medical Center)

  • Shrikanth Gadad

    (University of Texas Southwestern Medical Center)

  • Sang-Cheol Kim

    (Center for Genome Science, National Institute of Health, KCDC)

  • Mi-Young Kim

    (Korea Advanced Institute of Science and Technology (KAIST)
    KAIST Institute for the BioCentury, Cancer Metastasis Control Center)

Abstract

Some polypeptide N-acetyl-galactosaminyltransferases (GALNTs) are associated with cancer, but their function in organ-specific metastasis remains unclear. Here, we report that GALNT14 promotes breast cancer metastasis to the lung by enhancing the initiation of metastatic colonies as well as their subsequent growth into overt metastases. Our results suggest that GALNT14 augments the self-renewal properties of breast cancer cells (BCCs). Furthermore, GALNT14 overcomes the inhibitory effect of lung-derived bone morphogenetic proteins (BMPs) on self-renewal and therefore facilitates metastasis initiation within the lung microenvironment. In addition, GALNT14 supports continuous growth of BCCs in the lung by not only inducing macrophage infiltration but also exploiting macrophage-derived fibroblast growth factors (FGFs). Finally, we identify KRAS-PI3K-c-JUN signalling as an upstream pathway that accounts for the elevated expression of GALNT14 in lung-metastatic BCCs. Collectively, our findings uncover an unprecedented role for GALNT14 in the pulmonary metastasis of breast cancer and elucidate the underlying molecular mechanisms.

Suggested Citation

  • Ki-Hoon Song & Mi So Park & Tulip S. Nandu & Shrikanth Gadad & Sang-Cheol Kim & Mi-Young Kim, 2016. "GALNT14 promotes lung-specific breast cancer metastasis by modulating self-renewal and interaction with the lung microenvironment," Nature Communications, Nature, vol. 7(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13796
    DOI: 10.1038/ncomms13796
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