review · Pharmaceuticals
Recent advances in single-cell multi-omics integrate genomic, transcriptomic, proteomic, and metabolomic data at single-cell resolution. This approach allows researchers to decipher the complex cellular heterogeneity within the tumour microenvironment. It details the reciprocal interactions between cancer cells, cancer-associated fibroblasts, immune cells, and endothelial cells that influence tumour behaviour. Detailed investigations have highlighted critical immune evasion pathways, such as T cell exhaustion and hypoxia-driven metabolic reprogramming. They also expose mechanisms of therapeutic resistance linked to stromal cell secretions and physical barriers in the extracellular matrix. Integrating single-cell multi-omics with spatial relationships helps clarify how diversity within the microenvironment shapes treatment responses, offering insights that can inform the design of targeted and personalised cancer interventions.
Tumours are complex mixtures of various cell types that frequently adapt to survive standard treatments. By examining individual cells and their surrounding environment simultaneously, scientists can identify exactly how cancer cells evade the immune system and resist drugs. This level of biological detail is essential for creating more effective, personalised cancer treatments.
The insights outlined could inform the development of targeted cancer therapies, improved drug delivery systems, and enhanced immunotherapies. Potential users include oncology drug developers and clinical researchers seeking to overcome treatment resistance. As this work is a review synthesising biological mechanisms and future directions, the underlying concepts remain at an early, exploratory research stage.
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Recent developments in single-cell multi-omics technologies have provided the ability to identify diverse cell types and decipher key components of the tumor microenvironment (TME), leading to important advancements toward a much deeper understanding of how tumor microenvironment heterogeneity contributes to cancer progression and therapeutic resistance. These technologies are able to integrate data from molecular genomic, transcriptomic, proteomics, and metabolomics studies of cells at a single-cell resolution scale that give rise to the full cellular and molecular complexity in the TME. Understanding the complex and sometimes reciprocal relationships among cancer cells, CAFs, immune cells, and ECs has led to novel insights into their immense heterogeneity in functions, which can have important consequences on tumor behavior. In-depth studies have uncovered immune evasion mechanisms, including the exhaustion of T cells and metabolic reprogramming in response to hypoxia from cancer cells. Single-cell multi-omics also revealed resistance mechanisms, such as stromal cell-secreted factors and physical barriers in the extracellular matrix. Future studies examining specific metabolic pathways and targeting approaches to reduce the heterogeneity in the TME will likely lead to better outcomes with immunotherapies, drug delivery, etc., for cancer treatments. Future studies will incorporate multi-omics data, spatial relationships in tumor micro-environments, and their translation into personalized cancer therapies. This review emphasizes how single-cell multi-omics can provide insights into the cellular and molecular heterogeneity of the TME, revealing immune evasion mechanisms, metabolic reprogramming, and stromal cell influences. These insights aim to guide the development of personalized and targeted cancer therapies, highlighting the role of TME diversity in shaping tumor behavior and treatment outcomes.
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DOI: 10.3390/ph18010075
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