Journal
ONCOGENE
Volume 35, Issue 39, Pages 5170-5178Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2016.49
Keywords
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Funding
- Cancer League of Colorado CCTSI Mentored Career Development Award [1KL2TR001080-01]
- CCTSI CO PILOT NIH/NCI [M-13-161, 1R21CA185226-01]
- University of Colorado Cancer Center Summer Fellowship
- Cancer League of Colorado
- [U01CA153086]
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Understanding what drives breast tumor progression is of utmost importance for blocking tumor metastasis; we have identified that semaphorin 7a is a potent driver of ductal carcinoma in situ (DCIS) progression. Semaphorin 7a is a glycophosphatidylinositol membrane-anchored protein that promotes attachment and spreading in multiple cell types. Here, we show that increased expression of SEMA7A occurs in a large percentage of breast cancers and is associated with decreased overall and distant metastasis-free survival. In both in vitro and in vivo models, short hairpin-mediated silencing of SEMA7A reveals roles for semaphorin 7a in the promotion of DCIS growth, motility and invasion as well as lymphangiogenesis in the tumor microenvironment. Our studies also uncover a relationship between COX-2 and semaphorin 7a expression and suggest that semaphorin 7a promotes tumor cell invasion on collagen and lymphangiogenesis via activation of beta(1)-integrin receptor. Our results suggest that semaphorin 7a may be novel target for blocking breast tumor progression.
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