Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 188, Issue 4, Pages 1094-1103Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2017.12.009
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Funding
- NHLBI/NIH [HL084396, HL103868]
- Samuel Oschin Comprehensive Cancer Institute Lung Cancer Research Award
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR001881] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K08HL084396, R01HL123899, R01HL137076, R01HL120947, R01HL103868] Funding Source: NIH RePORTER
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Syndecan-1 is a transmembrane proteoglycan expressed prominently by lung epithelium and has pleiotropic functions such as regulating cell migration, proliferation, and survival. Loss of syndecan-1 expression by lung cancer cells is associated with higher-grade cancers and worse clinical prognosis. We evaluated the effects of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was moderated by syndecan-1. We also demonstrate that syndecan-1 (or lack thereof) alters the miRNA cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identified a distinct shift toward augmented procancer signaling consistent with the changes found in lung adenocarcinoma. Collectively, our work identifies syndecan-1 as an important factor in lung cancer cells that shapes the tumor microenvironment through alterations in miRNA packaging within exosomes.
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