Cancer Dis: Skin aging alters extracellular matrix components and promotes melanoma metastasis

Skin changes are one of the most striking features of aging. Human skin, including the epidermal and dermal layers, contains many collagen-rich extracellular matrix components secreted by dermal fibroblasts. Young dermal fibroblasts secrete many extracellular matrix components, including proteoglycans, glycoproteins, and cartilage connexins. HAPLN1 is a hyaluronic acid and proteoglycan connexin and is the most abundant protein component in the secreted extracellular matrix component.
Recently, researchers from the US Weststar Institute found that HAPLN1 is deleted in senescent fibroblasts, resulting in structural changes in the extracellular matrix that promote melanoma cell metastasis. The study further replenished HAPLN1 in the aging microenvironment, 3D skin reconstruction model and in vivo, and found that this treatment can inhibit the metastasis of cancer cells.
More interestingly, the researchers found that the extracellular matrix secreted by aging fibroblasts has an opposite effect on T cell migration and inhibits T cell migration. Treatment of senescent fibroblasts with HAPLN1 restores the ability of mononuclear immune cells to move, but blocks the movement of polymorphonuclear immune cells, which in turn affects the recruitment of Treg cells.
These data suggest that aging-related physical changes in the extracellular matrix can not only promote the migration of cancer cells, but also adversely affect the migration of some immune cells, leading to a comprehensive change in the immune microenvironment. An in-depth understanding of physical changes in aging skin may provide new insights into the treatment of elderly melanoma patients. The relevant research results were published in the international academic journal Cancer Discovery.
Reference materials:
Amanpreet Kaur, et al. Remodeling of the collagen matrix in aging skin promotes melanoma metastasis and affects immune cell motility. Cancer Discovery, DOI: 10.1158/2159-8290.CD-18-0193

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