Cell adhesion refers to a process of interaction and attachment between the surfaces of cells and neighboring cells mediated by some transmembrane proteins exerting functions of specialized cell surface receptors, also known as cell-adhesion molecules (CAMs). This process is shared by all multicellular organisms, and mostly occurs when cells attach to the surrounding extracellular matrix (ECM), a gel-like structure that contains molecules released by cells. Adhesion is achieved by indirect interactions, and specialized direct cell-cell junctions, including adherens junctions, gap junctions, tight junctions, desmosomes, etc. In addition to physically establishing connections between cells, these junctions also participate in the organization and regulation on elements of cytoskeleton, and serve as modulators of various signaling pathways.
Cell adhesion is fundamental for homeostasis in healthy tissues and is crucial in many biological activities, including cell communication, cell migration, tissue and organ formation, embryonic development, wound healing, and immune responses. Abnormal changes in cell adhesion are observed in a broad spectrum of diseases, such as cancers, arthritis, atherosclerosis, and osteoporosis.
Cell-to-cell adhesion and cell-to-matrix adhesion are both dependent on cell CAMs, which are mainly transmembrane proteins and generally contain 3 domains: a transmembrane domain, an intracellular domain, and an extracellular domain. CAMs are thus crucial in the proper development, plasticity, and structure and function maintenance of organs and tissues. According to sequences and structures of CAM proteins, cell adhesion molecules can be classified into 4 major groups: integrins, cadherins, immunoglobulins (Igs), and selectins. CAMs also serve as signaling effector molecules, forming a complex regulation network associated many signaling pathways, modulating a variety of cell activities, including proliferation, growth, differentiation, survival, motion, etc. The cross-regulation systems are composed of the ECM, cell adhesion molecules, and cell-secreted components, like cytokines or growth factors.
For example, it is demonstrated that integrins bind to LLC on ECM and release TGF-β, thus triggering Smad2/3, and then bind to the co-mediator Smad4 to provoke target genes, while inhibitory Smad (Smad6/7) inhibits this process. TGF-β is also involved in the activation of different downstream signaling pathways, including PI3K/AKT, Erk1/2, and p38 MAPK, to partake in the modification of pathways.
Fig.1 Crosstalk between the TGF-β and cell adhesion.1
Dysfunction of cell adhesion frequently occurs in cancer metastasis, allowing metastatic tumor cells to escape their site of origin and spread to the circulatory system. Indeed, loss of cell adhesion and anchorage-independent growth, are both dependent on CAMs, which are two important hallmarks of cancers. CAMs also function in thrombosis and inflammation, making them emerge as promising therapeutic targets for clinical research and drug development.
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