ITLN1 modulates invasive potential and metabolic reprogramming of ovarian cancer cells in omental microenvironment

Chi-Lam Au-Yeung (), Tsz-Lun Yeung, Abhinav Achreja, Hongyun Zhao, Kay-Pong Yip, Suet-Ying Kwan, Michaela Onstad, Jianting Sheng, Ying Zhu, Dodge L. Baluya, Ngai-Na Co, Angela Rynne-Vidal, Rosemarie Schmandt, Matthew L. Anderson, Karen H. Lu, Stephen T. C. Wong, Deepak Nagrath () and Samuel C. Mok ()
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Chi-Lam Au-Yeung: The University of Texas MD Anderson Cancer Center
Tsz-Lun Yeung: The University of Texas MD Anderson Cancer Center
Abhinav Achreja: University of Michigan
Hongyun Zhao: University of Michigan
Kay-Pong Yip: University of South Florida
Suet-Ying Kwan: The University of Texas MD Anderson Cancer Center
Michaela Onstad: The University of Texas MD Anderson Cancer Center
Jianting Sheng: Houston Methodist Research Institute, Weill Cornell Medicine
Ying Zhu: Houston Methodist Research Institute, Weill Cornell Medicine
Dodge L. Baluya: The University of Texas MD Anderson Cancer Center
Ngai-Na Co: The University of Texas MD Anderson Cancer Center
Angela Rynne-Vidal: The University of Texas MD Anderson Cancer Center
Rosemarie Schmandt: The University of Texas MD Anderson Cancer Center
Matthew L. Anderson: Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine
Karen H. Lu: The University of Texas MD Anderson Cancer Center
Stephen T. C. Wong: Houston Methodist Research Institute, Weill Cornell Medicine
Deepak Nagrath: University of Michigan
Samuel C. Mok: The University of Texas MD Anderson Cancer Center

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract Advanced ovarian cancer usually spreads to the omentum. However, the omental cell-derived molecular determinants modulating its progression have not been thoroughly characterized. Here, we show that circulating ITLN1 has prognostic significance in patients with advanced ovarian cancer. Further studies demonstrate that ITLN1 suppresses lactotransferrin’s effect on ovarian cancer cell invasion potential and proliferation by decreasing MMP1 expression and inducing a metabolic shift in metastatic ovarian cancer cells. Additionally, ovarian cancer-bearing mice treated with ITLN1 demonstrate marked decrease in tumor growth rates. These data suggest that downregulation of mesothelial cell-derived ITLN1 in the omental tumor microenvironment facilitates ovarian cancer progression.

Date: 2020
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DOI: 10.1038/s41467-020-17383-2

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