Journal
CANCER CELL
Volume 26, Issue 1, Pages 77-91Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2014.05.002
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Funding
- Ovarian Cancer Research Fund, Inc.
- Foundation for Women's Cancer
- Cancer Prevention Research Institute Texas (CPRIT) training grants [RP101502, RP101489]
- NIH T32 Training Grant [CA101642]
- Ann Schreiber Program for Excellence grant from the Ovarian Cancer Research Foundation
- Marsha Rivkin Center for Ovarian Cancer Research
- NIH [P50CA083639, CA109298, P50CA098258, CA177909, U54CA151668, UH2TR000943, CA016672, U54CA96300, U54CA96297]
- CPRIT [RP110595, RP120214]
- Ovarian Cancer Research Fund Program Project Development Grant
- Department of Defense [OC120547, OC093416]
- Betty Ann Asche Murray Distinguished Professorship
- Marcus Foundation
- RGK Foundation
- Gilder Foundation
- Judi A. Rees Ovarian Cancer Research Fund
- Chapman Foundation
- Meyer and Ida Gordon Foundation
- Ann Rife Cox Chair in Gynecology
- Blanton-Davis Ovarian Cancer Research Program
- Small Animal Imaging Facility
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Ovarian cancer has a clear predilection for metastasis to the omentum, but the underlying mechanisms involved in ovarian cancer spread are not well understood. Here, we used a parabiosis model that demonstrates preferential hematogenous metastasis of ovarian cancer to the omentum. Our studies revealed that the ErbB3-neuregulin 1 (NRG1) axis is a dominant pathway responsible for hematogenous omental metastasis. Elevated levels of ErbB3 in ovarian cancer cells and NRG1 in the omentum allowed for tumor cell localization and growth in the omentum. Depletion of ErbB3 in ovarian cancer impaired omental metastasis. Our results highlight hematogenous metastasis as an important mode of ovarian cancer metastasis. These findings have implications for designing alternative strategies aimed at preventing and treating ovarian cancer metastasis.
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