Abstract
Chronic inflammatory mediators exert pleiotropic effects in the development of cancer. On the one hand, inflammation favors carcinogenesis, malignant transformation, tumor growth, invasion, and metastatic spread; on the other hand inflammation can stimulate immune effector mechanisms that might limit tumor growth. The link between cancer and inflammation depends on intrinsic and extrinsic pathways. Both pathways result in the activation of transcription factors such as NF-κB, STAT-3, and HIF-1 and in accumulation of tumorigenic factors in tumor and microenvironment. STAT-3 and NF-κB interact at multiple levels and thereby boost tumor-associated inflammation which can suppress anti-tumor immune responses. These factors also promote tumor growth, progression, and metastatic spread. IL-1, IL-6, TNF, and PGHS-2 are key mediators of an inflammatory milieu by modulating the expression of tumor-promoting factors. In this review we concentrate on the crucial role of pro-inflammatory mediators in inflammation-driven carcinogenesis and outline molecular mechanisms of IL-1 signaling in tumors. In addition, we elucidate the dual roles of stress proteins as danger signals in the development of anti-cancer immunity and anti-apoptotic functions.
Highlights
Based on the presence of leukocytes in cancerous lesions, Rudolf Virchow, the founder of cellular pathology, speculated about an association between chronic inflammation and development of cancer already in 1863 (Virchow, 1863)
Apart from toxins, oncoproteins and growth factors can affect the host via an activation of pattern recognition receptors (PRR) that interact with pathogen-associated molecular patterns (PAMP)
These receptors comprise to members of the Toll-like receptor (TLR) family, nucleotide-binding oligomerization domain-like (NODlike) receptors (NLR), C-type lectin receptors (CLR), triggering receptors on myeloid cells (TREM), and retinoic acid inducible gene-I-like receptors (RLR; Kawai and Akira, 2011)
Summary
Edited by: Cristina Bonorino, Pontificia Universidade Catolica do Rio Grande do Sul, Brazil. Reviewed by: Lidija Klampfer, Montefiore Medical Center and Albert Einstein Cancer Center, USA Ana Paula Souza, Pontificia Universidade Católica do Rio Grande do Sul, Brazil. The link between cancer and inflammation depends on intrinsic and extrinsic pathways Both pathways result in the activation of transcription factors such as NF-κB, STAT-3, and HIF-1 and in accumulation of tumorigenic factors in tumor and microenvironment. STAT-3 and NF-κB interact at multiple levels and thereby boost tumor-associated inflammation which can suppress anti-tumor immune responses. These factors promote tumor growth, progression, and metastatic spread. In this review we concentrate on the crucial role of pro-inflammatory mediators in inflammation-driven carcinogenesis and outline molecular mechanisms of IL-1 signaling in tumors.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
