review · International Journal of Molecular Sciences
Research into colorectal cancer increasingly focuses on the tumour microenvironment alongside tumour cell genetics. The invasive nature of primary colorectal cancer is driven both by cancer cell genotypes and by interactions with the surrounding extracellular setting. Cells within the tumour microenvironment can exert conflicting effects, functioning in both pro-tumour and anti-tumour capacities. Interactions between tumour-infiltrating cells and cancer cells cause these infiltrating cells to polarise into opposing phenotypes. Multiple interconnected oncogenic and tumour-suppressing signalling pathways regulate this process. The dual functions and complex relationships among these components frequently undermine colorectal cancer management. A clearer grasp of these cellular pathways and microenvironmental components outlines potential routes for creating targeted, effective colorectal cancer therapies.
Colorectal cancer remains difficult to control because the surrounding tissue contains cells that can either fight or promote tumours. Unravelling the contradictory signalling pathways that direct these cells provides essential biological insight. This understanding helps clarify why existing treatments fail and assists researchers in designing more targeted therapeutic strategies.
This research outlines foundational biological mechanisms to inform future personalized colorectal cancer therapies. Potential users include pharmaceutical developers and translational oncology researchers seeking new drug targets. As a review of cellular interactions and signalling pathways, the work remains at an early discovery stage, far from direct commercial deployment.
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The study of the tumor microenvironment (TME) has become an important part of colorectal cancer (CRC) research. Indeed, it is now accepted that the invasive character of a primary CRC is determined not only by the genotype of the tumor cells, but also by their interactions with the extracellular environment, which thereby orchestrates the development of the tumor. In fact, the TME cells are a double-edged sword as they play both pro- and anti-tumor roles. The interaction of the tumor-infiltrating cells (TIC) with the cancer cells induces the polarization of the TIC, exhibiting an antagonist phenotype. This polarization is controlled by a plethora of interconnected pro- and anti-oncogenic signaling pathways. The complexity of this interaction and the dual function of these different actors contribute to the failure of CRC control. Thus, a better understanding of such mechanisms is of great interest and provides new opportunities for the development of personalized and efficient therapies for CRC. In this review, we summarize the signaling pathways linked to CRC and their implication in the development or inhibition of the tumor initiation and progression. In the second part, we enlist the major components of the TME and discuss the complexity of their cells functions.
This page summarises published work. The authoritative version sits with the publisher.
DOI: 10.3390/ijms24065600
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