Mutant B-Raf(V600E) promotes melanoma paracellular transmigration by inducing thrombin-mediated endothelial junction breakdown

Pu Zhang; Shan Feng; Gentao Liu; Heyong Wang; Huifeng Zhu; Qiao Ren; Huiyuan Bai; Changliang Fu; Cheng Dong

doi:10.1074/jbc.M115.696419

Mutant B-Raf(V600E) promotes melanoma paracellular transmigration by inducing thrombin-mediated endothelial junction breakdown

Pu Zhang, Shan Feng, Gentao Liu, Heyong Wang, Huifeng Zhu, Qiao Ren, Huiyuan Bai, Changliang Fu, Cheng Dong

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

Background: A prothrombotic state is one of the hallmarks of advanced cancer. Results: B-Raf(V600E)-dependent thrombin release from metastatic melanoma signals focal adherens junction disassembly by triggering VE-cadherin phosphorylation and ubiquitination. Conclusion: Thrombin-mediated junction breakdown allows melanoma extravasation via a paracellular route. Significance: Targeting B-Raf(V600E)-mediated thrombin generation and endothelial barrier dysfunction may represent a novel therapeutic strategy to limit tumor metastasis.

Original language	English (US)
Pages (from-to)	2087-2106
Number of pages	20
Journal	Journal of Biological Chemistry
Volume	291
Issue number	5
DOIs	https://doi.org/10.1074/jbc.M115.696419
State	Published - Jan 29 2016

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Biology
Cell Biology

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10.1074/jbc.M115.696419

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title = "Mutant B-Raf(V600E) promotes melanoma paracellular transmigration by inducing thrombin-mediated endothelial junction breakdown",

abstract = "Background: A prothrombotic state is one of the hallmarks of advanced cancer. Results: B-Raf(V600E)-dependent thrombin release from metastatic melanoma signals focal adherens junction disassembly by triggering VE-cadherin phosphorylation and ubiquitination. Conclusion: Thrombin-mediated junction breakdown allows melanoma extravasation via a paracellular route. Significance: Targeting B-Raf(V600E)-mediated thrombin generation and endothelial barrier dysfunction may represent a novel therapeutic strategy to limit tumor metastasis.",

author = "Pu Zhang and Shan Feng and Gentao Liu and Heyong Wang and Huifeng Zhu and Qiao Ren and Huiyuan Bai and Changliang Fu and Cheng Dong",

note = "Publisher Copyright: {\textcopyright} 2016 by The American Society for Biochemistry and Molecular Biology, Inc. Published in the U.S.A.",

year = "2016",

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doi = "10.1074/jbc.M115.696419",

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TY - JOUR

T1 - Mutant B-Raf(V600E) promotes melanoma paracellular transmigration by inducing thrombin-mediated endothelial junction breakdown

AU - Zhang, Pu

AU - Feng, Shan

AU - Liu, Gentao

AU - Wang, Heyong

AU - Zhu, Huifeng

AU - Ren, Qiao

AU - Bai, Huiyuan

AU - Fu, Changliang

AU - Dong, Cheng

PY - 2016/1/29

Y1 - 2016/1/29

N2 - Background: A prothrombotic state is one of the hallmarks of advanced cancer. Results: B-Raf(V600E)-dependent thrombin release from metastatic melanoma signals focal adherens junction disassembly by triggering VE-cadherin phosphorylation and ubiquitination. Conclusion: Thrombin-mediated junction breakdown allows melanoma extravasation via a paracellular route. Significance: Targeting B-Raf(V600E)-mediated thrombin generation and endothelial barrier dysfunction may represent a novel therapeutic strategy to limit tumor metastasis.

AB - Background: A prothrombotic state is one of the hallmarks of advanced cancer. Results: B-Raf(V600E)-dependent thrombin release from metastatic melanoma signals focal adherens junction disassembly by triggering VE-cadherin phosphorylation and ubiquitination. Conclusion: Thrombin-mediated junction breakdown allows melanoma extravasation via a paracellular route. Significance: Targeting B-Raf(V600E)-mediated thrombin generation and endothelial barrier dysfunction may represent a novel therapeutic strategy to limit tumor metastasis.

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Mutant B-Raf(V600E) promotes melanoma paracellular transmigration by inducing thrombin-mediated endothelial junction breakdown

Abstract

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