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Review
. 2022 Jun 13:2022:3128933.
doi: 10.1155/2022/3128933. eCollection 2022.

Tumor-Associated Inflammation: The Tumor-Promoting Immunity in the Early Stages of Tumorigenesis

Qing Bi  1   2 , Ji-Yue Wu  1   2 , Xue-Meng Qiu  3 , Jian-Dong Zhang  1   2 , Ze-Jia Sun  1   2 , Wei Wang  1   2
Affiliations
Review

Tumor-Associated Inflammation: The Tumor-Promoting Immunity in the Early Stages of Tumorigenesis

Qing Bi et al. J Immunol Res. .

Abstract

Tumorigenesis is a multistage progressive oncogenic process caused by alterations in the structure and expression level of multiple genes. Normal cells are continuously endowed with new capabilities in this evolution, leading to subsequent tumor formation. Immune cells are the most important components of inflammation, which is closely associated with tumorigenesis. There is a broad consensus in cancer research that inflammation and immune response facilitate tumor progression, infiltration, and metastasis via different mechanisms; however, their protumor effects are equally important in tumorigenesis at earlier stages. Previous studies have demonstrated that during the early stages of tumorigenesis, certain immune cells can promote the formation and proliferation of premalignant cells by inducing DNA damage and repair inhibition, releasing trophic/supporting signals, promoting immune escape, and activating inflammasomes, as well as enhance the characteristics of cancer stem cells. In this review, we focus on the potential mechanisms by which immune cells can promote tumor initiation and promotion in the early stages of tumorigenesis; furthermore, we discuss the interaction of the inflammatory environment and protumor immune cells with premalignant cells and cancer stem cells, as well as the possibility of early intervention in tumor formation by targeting these cellular mechanisms.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Steps of tumorigenesis and the hallmarks of cancer. A normal cell is transformed into cell-of-origin (COO) after receiving the first oncogenic mutation (tumor initiation). COOs subsequently develop into pre-malignant cells (tumor promotion) and undergo the malignant conversion; they finally enter the tumor progression stage (including tumor infiltration, invasion, and metastasis). During the process, cancers obtain a series of hallmarks and characteristics involving “sustaining proliferative signaling,” “evading growth suppressors,” “resisting cell death,” “enabling replicative immortality,” “inducing or accessing vasculature,” “activating invasion and metastasis,” “deregulating cellular metabolism,” “avoiding immune destruction,” “unlocking phenotypic plasticity,” “nonmutational epigenetic reprogramming,” “polymorphic microbiomes,” and “senescent cells.”
Figure 2
Figure 2
Tumor-promoting immune microenvironment in the early stages of tumorigenesis. Immune cell-mediated tumor-promoting mechanisms involve driving DNA damage and repair inhibition, releasing proliferation signals, inducing immune escape, enhancing characteristics of cancer stem cells, and activating inflammasomes. DUOX, dual oxidase; mPGES, microsomal prostaglandin E synthase; P2RY12, purinergic receptor P2Y12; OA, osteoactivin; ST2, suppression of tumorigenicity 2; MR1, MHC class I-related protein 1; NOX2, NADPH oxidase 2; GABA, gamma-aminobutyric acid; STAT3, signal transducer and activator of transcription 3; G-CSF, granulocyte colony-stimulating factor; DOT1L, disruptor of telomeric silencing 1-like; BMP2, bone morphogenetic protein 2; MDSC, myeloid-derived suppressor cell; Treg, regulatory T cell; Breg, regulatory B cell; MAIT cell, Mucosal-associated invariant T cell; DC, dendritic cell.
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