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Review
. 2023 Sep 21;24(18):14390.
doi: 10.3390/ijms241814390.

A Route for Investigating Psoriasis: From the Perspective of the Pathological Mechanisms and Therapeutic Strategies of Cancer

Xingkang Wu  1 , Yushuang Ma  1 , Lu Wang  1 , Xuemei Qin  1
Affiliations
Review

A Route for Investigating Psoriasis: From the Perspective of the Pathological Mechanisms and Therapeutic Strategies of Cancer

Xingkang Wu et al. Int J Mol Sci. .

Abstract

Psoriasis is an incurable skin disease that develops in about two-thirds of patients before the age of 40 and requires lifelong treatment; its pathological mechanisms have not been fully elucidated. The core pathological process of psoriasis is epidermal thickening caused by the excessive proliferation of epidermal keratinocytes, which is similar to the key feature of cancer; the malignant proliferation of cancer cells causes tumor enlargement, suggesting that there is a certain degree of commonality between psoriasis and cancer. This article reviews the pathological mechanisms that are common to psoriasis and cancer, including the interaction between cell proliferation and an abnormal immune microenvironment, metabolic reprogramming, and epigenetic reprogramming. In addition, there are common therapeutic agents and drug targets between psoriasis and cancer. Thus, psoriasis and cancer share a common pathological mechanisms-drug targets-therapeutic agents framework. On this basis, it is proposed that investigating psoriasis from a cancer perspective is beneficial to enriching the research strategies related to psoriasis.

Keywords: cancer; cell proliferation; immune microenvironment; psoriasis.

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Conflict of interest statement

The authors declare that they have no known competing financial interest or personal relationship that could have appeared to influence the work reported in this paper.

Figures

Figure 1
Figure 1
The positive feedback loop of a keratinocyte-immune microenvironment. TNF-α: tumor necrosis factor alpha; INF-γ: interferon-gamma; IL-17: interleukin-17; IL-22: interleukin-22.
Figure 2
Figure 2
Comparison of the interaction between cell proliferation and immune microenvironment in psoriasis and cancer. DC cells: dendritic cells; IL-12: interleukin-12; IL-23: interleukin-23; Th1 cells: T helper 1 cells; Th17 cells: T helper 17 cells; Th22 cells: T helper 22 cells; TNF-α: tumor necrosis factor alpha; INF-γ: interferon gamma; IL-17: interleukin-17; IL-6: interleukin-6; IL-1β: interleukin-1β; TGFβ: transforming growth factor-β; ILC3 cells: group 3 innate lymphoid cells; γδ T cells: gamma delta T cells; IL-1: interleukin-1; IL-8: interleukin-8; IL-13: interleukin-13; IL-35: interleukin-35; IL-33: interleukin-33; IL-11: interleukin-11.
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