Abstract
Simple SummaryTumours are not formed only by malignant cells but contain many other cell types, including endothelial and mural cells of blood vessels, immune cells and cancer-associated fibroblasts. These host cells, together with extracellular matrix, form the tumour stroma. Tumour growth and metastasis depends on interactions between cancer cells and tumour stroma. Cell adhesion to extracellular matrix is essential for tissue growth and homeostasis and is deregulated in many pathological conditions, including cancer. This review highlights the vital role of cell adhesion in malignancy and describes how adhesion components regulate tumour stroma responses and control cancer development.Beyond the conventional perception of solid tumours as mere masses of cancer cells, advanced cancer research focuses on the complex contributions of tumour-associated host cells that are known as “tumour microenvironment” (TME). It has been long appreciated that the tumour stroma, composed mainly of blood vessels, cancer-associated fibroblasts and immune cells, together with the extracellular matrix (ECM), define the tumour architecture and influence cancer cell properties. Besides soluble cues, that mediate the crosstalk between tumour and stroma cells, cell adhesion to ECM arises as a crucial determinant in cancer progression. In this review, we discuss how adhesome, the intracellular protein network formed at cell adhesions, regulate the TME and control malignancy. The role of adhesome extends beyond the physical attachment of cells to ECM and the regulation of cytoskeletal remodelling and acts as a signalling and mechanosensing hub, orchestrating cellular responses that shape the tumour milieu.
Highlights
Malignant cells are the main driving force of tumour formation and growth, yet they do not manifest the disease single-handed
Unique markers for cancer-associated fibroblasts (CAFs) have not been defined, and CAFs are mainly recognised by the expression of myofibroblast proteins, such as a-smooth muscle actin, fibroblast activation protein (FAP), fibroblast-specific protein 1 (FSP1), and vimentin [195]
We classify Tumour-infiltrating immune cells (TICs) into two main categories according to their recruitment in innate, or adaptive (T and B lymphocytes) immune responses to review the role of adhesome components in immune tumour microenvironment (TME) composition and function
Summary
Malignant cells are the main driving force of tumour formation and growth, yet they do not manifest the disease single-handed. It is increasingly accepted that noncancerous cells located in the tumour niche are involved in the hallmark capabilities of cancer [1]. Key cellular players in the tumour stroma are vascular cells comprising blood and lymphatic vessels (endothelial cells and mural cells), cancer-associated fibroblasts (CAFs), and infiltrating immune cells. Additional stromal cell types of solid tumours include mesenchymal stem cells, adipocytes and neurons [2,3]. The complex contributions of these allegedly normal, constituent cells together with noncellular components, namely the extracellular matrix (ECM) and soluble factors, are collectively known as the tumour microenvironment (TME) (Figure 1).
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