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Roles of tumor suppressors in regulating tumor-associated inflammation
1Laboratory of Cancer Biology and Genetics, National Cancer Institute, NIH, 37 Convent Drive, Bethesda, MD, USA.
Abstract:
Loss or silencing of tumor suppressors (TSs) promotes neoplastic transformation and malignant progression. To date, most work on TS has focused on their cell autonomous effects. Recent evidence, however, demonstrates an important noncell autonomous role for TS in the control of tumor-associated inflammation. We review evidence from clinical data sets and mouse model studies demonstrating enhanced inflammation and altered tumor microenvironment (TME) upon TS inactivation. We discuss clinical correlations between tumor-associated inflammation and inactivation of TS, and their therapeutic implications. This review sets forth the concept that TS can also suppress tumor-associated inflammation, a concept that provides new insights into tumor-host interactions. We also propose that in some cases the loss of TS function in cancer can be overcome through inhibition of the resulting inflammatory response, regardless whether it is a direct or an indirect consequence of TS loss.
Insights
Loss of tumor suppressors (TSs) not only drives cancer but also fuels tumor-associated inflammation. Targeting this inflammation, a non-cell autonomous effect of TS loss, offers new therapeutic strategies for cancer treatment.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Tumor suppressors (TSs) are critical in preventing cancer, with research traditionally focusing on their cell-autonomous functions.
- Emerging evidence highlights a significant non-cell autonomous role for TSs in regulating tumor-associated inflammation.
- Inactivation of TSs is increasingly linked to an altered tumor microenvironment (TME) and heightened inflammation.
Purpose of the Study:
- To review the evidence for TSs' role in controlling tumor-associated inflammation.
- To explore the clinical correlations between TS inactivation, inflammation, and therapeutic strategies.
- To introduce the concept of TSs as suppressors of tumor-associated inflammation and discuss its implications for tumor-host interactions.
Main Methods:
- Review of clinical datasets.
- Analysis of mouse model studies.
- Synthesis of existing literature on TSs and inflammation.
Main Results:
- TS inactivation is associated with enhanced inflammation and a modified tumor microenvironment (TME).
- Clinical data show correlations between tumor-associated inflammation and TS inactivation.
- TSs play a role in suppressing inflammation, impacting tumor-host interactions.
Conclusions:
- TSs possess a non-cell autonomous function in suppressing tumor-associated inflammation.
- The inflammatory response resulting from TS loss can be therapeutically targeted.
- Understanding this inflammatory role of TSs offers novel insights and potential therapeutic avenues in cancer treatment.
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