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CD43 (sialophorin) is involved in the induction of extracellular matrix remodeling and angiogenesis by lung cancer cells
Aberrant expression of CD43 in malignant tumors of nonhematopoietic origin such as those from lung, cervix, colon, and breast has been shown to correlate with poor prognosis, providing tumor cells with enhanced motility, anchorage‐independent growth, and in vivo tumor size, while protecting the cell...
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Published in: | Journal of cellular physiology 2021-09, Vol.236 (9), p.6643-6656 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Aberrant expression of CD43 in malignant tumors of nonhematopoietic origin such as those from lung, cervix, colon, and breast has been shown to correlate with poor prognosis, providing tumor cells with enhanced motility, anchorage‐independent growth, and in vivo tumor size, while protecting the cells of NK lysis and apoptosis. To further characterize the role of CD43 in cell transformation, we tested whether interfering its expression modified the capacity of the A549 non‐small cell lung cancer cells to secrete molecules contributing to malignancy. The proteomic analysis of the secretome of serum‐starved A549 cells revealed that cells expressing normal levels of CD43 released significantly high levels of molecules involved in extracellular matrix organization, angiogenesis, platelet degranulation, collagen degradation, and inflammation, as compared to CD43 RNAi cells. This data reveals a novel and unexpected role for CD43 in lung cancer development, mainly in remodeling the tumor microenvironment.
Proteomic analysis of A549 cells secretome reveals a novel role of CD43 in lung cancer development, mainly in the remodeling of the tumor microenvironment. Our study shows that cells expressing normal levels of CD43 released significantly higher levels of molecules involved in the extracellular matrix organization, angiogenesis, platelet degranulation, collagen degradation, and inflammation. |
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ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.30308 |