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Published on: July 26, 2017
S100A9 interaction with TLR4 promotes tumor growth
Eva Källberg1, Thomas Vogl, David Liberg
1Immunology Group, Lund University, Lund, Sweden.
Plos One
|April 4, 2012
Summary
Mice lacking S100A9 protein showed delayed tumor growth, suggesting S100A9 promotes cancer. Inhibiting the S100A9-TLR4 interaction with a small molecule also reduced tumor growth, indicating a potential new cancer therapy.
Area of Science:
- Oncology
- Immunology
Background:
- S100A9 is implicated in various cancers.
- The role of S100A9 in prostate tumor progression is not fully understood.
Purpose of the Study:
- To investigate the role of S100A9 in tumor growth.
- To explore the therapeutic potential of targeting S100A9-TLR4 interactions.
Main Methods:
- Utilized S100A9 knock-out (S100A9(-/-)) and Toll-like receptor 4 knock-out (TLR4(-/-)) TRAMP mice models.
- Analyzed S100A9 expression in mouse and human prostate tumor tissues.
- Assessed tumor growth inhibition in response to S100A9-TLR4 pathway modulation.
Main Results:
- S100A9 deficiency significantly delayed tumor growth in TRAMP mice.
- S100A9 was detected in tumor-associated macrophages (CD11b(+) and CD68(+)) but not in normal prostate tissue.
- Inhibition of S100A9-TLR4 interaction using ABR-215050 reduced tumor growth in EL-4 lymphoma models.
Conclusions:
- S100A9 and TLR4 play a role in promoting tumor growth.
- Targeting the S100A9-TLR4 pathway represents a promising anti-tumor therapeutic strategy.
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