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Danger matrix molecules orchestrate CD14/CD44 signaling in cancer development
Heiko Roedig1, Roxana Damiescu1, Jinyang Zeng-Brouwers1
1Pharmazentrum Frankfurt, Institut für Allgemeine Pharmakologie und Toxikologie, Goethe University, Frankfurt am Main, Germany.
Seminars in Cancer Biology
|August 15, 2019
Summary
Tumor matrix components like biglycan act as danger signals (DAMPs), influencing inflammation and autophagy via Toll-like receptors (TLRs). This explains how matrix molecules can either promote or suppress cancer growth.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- The tumor microenvironment, including inflammation and autophagy, is critical for cancer progression.
- Proteoglycans in the tumor stroma function as danger-associated molecular patterns (DAMPs) when soluble.
- DAMPs interact with Toll-like receptors (TLRs), initiating inflammation and modulating autophagy.
Purpose of the Study:
- To review and discuss the role of matrix-derived DAMPs (biglycan, hyaluronan, versican) in cancer.
- To elucidate the signaling dialogue between TLRs, CD14, and CD44 in regulating inflammation and autophagy.
- To explain the dual role of matrix-derived DAMPs in tumor growth promotion or suppression.
Main Methods:
- Literature review and critical discussion of existing research.
- Focus on mechanistic insights into signaling pathways.
- Emphasis on the interplay between biglycan, hyaluronan, and versican with TLRs, CD14, and CD44.
Main Results:
- Biglycan regulates the cross-talk between inflammation and autophagy by modulating TLR co-receptors CD14 and CD44.
- This signaling switch explains contradictory findings on DAMPs' effects on tumor growth.
- Matrix-derived DAMPs orchestrate a complex dialogue influencing cancer development.
Conclusions:
- Matrix-derived DAMPs are key regulators of the inflammation-autophagy axis in cancer.
- Understanding the TLR-, CD14-, and CD44-mediated signaling is crucial for cancer therapy.
- Biglycan, hyaluronan, and versican represent important targets for modulating cancer progression.
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