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Nat Commun: Unexpectedly, ultraviolet light can inhibit the invasion of melanoma

 Last Update: 2021-05-21
 Source: Internet
 Author: User

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collagen fibrils

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Ultraviolet rays are the main environmental risk factor for melanoma, and sunlight exposure is the main reason for the increase in disease incidence.

UV damage accumulates with the extension of life, and the survival rate of melanoma in elderly patients is worse.

Existing studies have shown that fibroblasts and their matrix contribute to the occurrence of cancer, so researchers have explored how ultraviolet light can change the function of dermal fibroblasts, the extracellular matrix (ECM) and the invasion of melanoma.

In this study, it was confirmed that UVR-injured fibroblasts continued to upregulate the expression of collagen scavenging matrix metalloprotein-1 (MMP1) and reduce local collagen (COL1A1), and that COL1A1 degraded by MMP1 reduced the invasion of melanoma .

UVR-injured fibroblasts continue to up-regulate collagen scavenging matrix metalloprotein-1 (MMP1) expression and reduce local collagen (COL1A1).

Decreased amount and integrity of collagen reduces the invasion of melanoma cells

Primary skin melanoma in the elderly shows more cancer cells as single-cell invasion, and more collagen is expressed and deposited at the front of the invasion of melanoma.

Invasion of collagen and single melanoma cells is a strong predictor of poor melanoma-specific survival rate Collagen and single melanoma cell invasion is a strong predictor of poor melanoma-specific survival rate

However, melanoma-related fibroblasts can restore invasion by increasing collagen synthesis.

Finally, the study proved that the high expression of the COL1A1 gene is a series of biomarkers for the adverse outcome of primary cancers .

The high expression of COL1A1 gene is a series of biomarkers for the adverse outcome of primary cancers The high expression of COL1A1 gene is a series of biomarkers for the adverse outcome of primary cancers

Original source:

Timothy Budden et al.

et al.

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