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Hematogenous Metastasis of Ovarian Cancer: Rethinking Mode of Spread

2014; Cell Press; Volume: 26; Issue: 1 Linguagem: Inglês

10.1016/j.ccr.2014.05.002

1878-3686

Sunila Pradeep, Seung Wook Kim, Sherry Y. Wu, Masato Nishimura, Pradeep Chaluvally‐Raghavan, Takahito Miyake, Chad V. Pecot, Sun-Jin Kim, Hyun Jin Choi, Farideh Z. Bischoff, Julie Ann Mayer, Li Huang, Alpa M. Nick, Carolyn Hall, Cristian Rodriguez‐Aguayo, Behrouz Zand, Heather J. Dalton, Thiruvengadam Arumugam, Ho Jeong Lee, Hee Dong Han, Min Soon Cho, Rajesha Rupaimoole, Lingegowda S. Mangala, Vasudha Sehgal, Sang Cheul Oh, Jinsong Liu, Ju‐Seog Lee, Robert L. Coleman, Prahlad T. Ram, Gabriel López-Berestein, Isaiah J. Fidler, Anil K. Sood,

Polyomavirus and related diseases

Summary 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.