Abstract

Cutaneous squamous cell carcinoma is the second most prevalent skin cancer worldwide (Que et al., 2018). Although UV exposure is the most common cause of cutaneous squamous cell carcinoma, polycyclic aromatic hydrocarbons, such as 7,12-dimethylbenz[a]anthracene (DMBA), remain causative agents. Epidermal Langerhans cells (LCs) capture DMBA that can penetrate the stratum corneum and generate the highly carcinogenic compound DMBA-3,4-diol-1,2-epoxide (Modi et al., 2012). The aryl hydrocarbon receptor/cytochrome P-450 pathway mediates the metabolic conversion of DMBA in the epidermis (Modi et al., 2012).

Highlights

  • Late cornified envelope proteins (Ishitsuka et al, 2016)

  • In the two-stage chemical carcinogenesis, LKO mice developed significantly more papillomas than wild-type mice subjected to low- and Abbreviations: CE, cornified envelope; dimethylbenz[a] anthracene (DMBA), 7,12-dimethylbenz[a]anthracene; EPI, envoplakin, periplakin, and involucrin; LC, Langerhans cell; LKO, LOR knockout; LOR, loricrin

  • NAcetyl cysteine treatment in LKO mice but not in wild-type mice significantly reduced the tumor burden compared with the vehicle-treated control group (Figure 2b)

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Summary

Introduction

Late cornified envelope proteins (Ishitsuka et al, 2016). Given the indispensable role of LOR in cornification and its potential antioxidative properties identified from previous research, we hypothesized that LOR may protect against the chemical carcinogen DMBA. NRF2 activation in FVB LKO mice (Ishitsuka et al, 2016), single topical Epidermis compared with that in the wild-type epidermis (Figure 1a).

Results
Conclusion
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