Abstract
Colorectal cancer remains one of the most important health challenges in our society. The development of cancer immunotherapies has fostered the need to better understand the anti-tumor immune mechanisms at play in the tumor microenvironment and the strategies by which the tumor escapes them. In this review, we provide an overview of the molecular interactions that regulate tumor inflammation. We particularly discuss immunomodulatory cell-cell interactions, cell-soluble factor interactions, cell-extracellular matrix interactions and cell-microbiome interactions. While doing so, we highlight relevant examples of tumor immunomodulation in colorectal cancer.
Highlights
Colorectal cancer is the second leading cause of cancer-related deaths in the world, accounting for nearly 1 million deaths in 2020
Whereas the majority of primary colorectal cancers can be eradicated through surgical resection, only a minority of patients diagnosed with metastatic CRC can be cured by surgery
We present multiple key of molecular occurring in the colorectal present multiple key molecular interactions occurring in the colorectal tumor microenvimicroenvironment (TME) that strongly modulate tumor inflammation
Summary
Colorectal cancer is the second leading cause of cancer-related deaths in the world, accounting for nearly 1 million deaths in 2020. Cancer of intestinal epithelial cells (IECs) to a benign adenoma, before progressing to malignancy cells actively remodel their microenvironment by interacting with immune cells, stromal upon of genetic and epigenetic aberrations. The primary tumor growthcells alters actively remodel microenvironment byintratumoral interacting with immuneofcells, stromal the integrity of their the gut barrier, leading to infiltration bacteria andcells other and the extracellular matrix (ECM). Cancer cells must undergo phenotypic changes that allow them to exit their cell cluster organization, acquire the capacity to penetrate blood or lymphatic vessels, and survive into circulation This process is referred as epithelial-to-mesenchymal transition (EMT), reflecting the loss of epithelial cell characteristics and the acquisition of a mesenchymal cell phenotype with enhanced invasive behavior.
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