Dynamic roles of inflammasomes in inflammatory tumor microenvironment

Abstract

The inflammatory tumor microenvironment has been known to be closely connected to all stages of cancer development, including initiation, promotion, and progression. Systemic inflammation in the tumor microenvironment is increasingly being recognized as an important prognostic marker in cancer patients. Inflammasomes are master regulators in the first line of host defense for the initiation of innate immune responses. Inflammasomes sense pathogen-associated molecular patterns and damage-associated molecular patterns, following recruitment of immune cells into infection sites. Therefore, dysregulated expression/activation of inflammasomes is implicated in pathogenesis of diverse inflammatory disorders. Recent studies have demonstrated that inflammasomes play a vital role in regulating the development and progression of cancer. This review focuses on fate-determining roles of the inflammasomes and the principal downstream effector cytokine, IL-1β, in the tumor microenvironment.

Lipidomic Typing of Colorectal Cancer Tissue Containing Tumour-Infiltrating Lymphocytes by MALDI Mass Spectrometry Imaging

“…To overcome these limitations, multiple means of performing subtyping of these cases are being investigated, with many approaches focusing on the presence of tumour infiltrating lymphocytes (TILs) given that an enhanced presence of certain TILs may indicate an improved prognosis and response to immunotherapy [17,18]. This may not be surprising considering that lymphocytic infiltration is a major immunological defence against tumour cells in solid tumours, especially in the microenvironment where inflammatory activity plays a key role in initiating an appropriate immune response [19,20]. In particular, several studies have shown that the number and type of TILs are prognostic indicators for disease-free survival in numerous malignancies, including CRC, and are also associated with the response of a tumour following treatment with traditional immunotherapy [21][22][23].…”

D-Dimer is a Predictive Factor of Cancer Therapeutics-Related Cardiac Dysfunction in Patients Treated With Cardiotoxic Chemotherapy

“…Although the precise mechanisms are still complex and uncovered, pro-coagulable state may produce a suitable milieu for cancer progression by recruitment of pro-metastatic leukocytes, adhesion to the endothelium, transendothelial migration, and restriction in natural killer cell-mediated clearance of micrometastasis [17,18]. Accumulating evidence showed that abnormal in ammation and oxidative stress are key factors to the development of heart failure, and those also play important roles in cancer progression and thrombus formation [19][20][21][22][23]. The in ammatory microenvironment is now recognized as an important participant or a regulator of all stages of tumor development, from an early stage of carcinogenesis to tumor promotion and metastatic spread to distant organs [22].…”

“…Accumulating evidence showed that abnormal in ammation and oxidative stress are key factors to the development of heart failure, and those also play important roles in cancer progression and thrombus formation [19][20][21][22][23]. The in ammatory microenvironment is now recognized as an important participant or a regulator of all stages of tumor development, from an early stage of carcinogenesis to tumor promotion and metastatic spread to distant organs [22]. Regarding to thrombus formation, Gomes et al reported that blockade of IL-1 receptor abolished the neutrophil extracellular traps-dependent prothrombotic state and attenuated cancer-associated thrombosis in murine breast cancer model [23].…”

Inhibitory Role of Berberine, an Isoquinoline Alkaloid, on NLRP3 Inflammasome Activation for the Treatment of Inflammatory Diseases

“…This establishes an inflammatory microenvironment, which promotes cancer progression and metastasis. The tumor-infiltrating immune cells, such as neutrophils, dendritic cells, and TAMs, further promote the secretion of IL-1β in the tumor microenvironment [ 27 ]. IL-1β secretion also contributes to angiogenesis by promoting the release of cytokines such as vascular endothelial growth factor (VEGF), macrophage-inflammatory protein-2 (CXCL2), and hepatocyte growth factor (HGF).…”

“…IL-1β has also shown to promote proliferation in cancer cells by activating several oncogenic signaling pathways [ 8 , 28 , 29 , 30 ]. In addition, extracellular ATP released from damaged tumor cells upon anti-cancer treatment also induces NLRP3 inflammasome activation [ 27 ]. Studies have suggested the role of IL-18 in the polarization of T cells toward Th1 or Th2 cells by inducing IL-17 expression in Th17 cells in certain types of cancer, while the role of IL-18 in tumor progression has not been fully elucidated yet [ 27 ].…”