Journal of Clinical and Aesthetic Dermatology - Science of Skin Summit 2025

109—3D organoid modeling reveals how hostmicrobiota interactions fuel skin cancer in the context of TLR4 deficiency and epithelial IKKa reduction

2025-10-29 08:30:02

Presenters: Singh AK1

Affiliations: 1Cancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, National Institute of Health, Frederick, MD

Background: Pattern recognition receptors (PRRs), such as Toll-like receptor 4 (TLR4), detect pathogen-associated molecular patterns (PAMPs) and help maintain epithelial homeostasis. While their roles in infection and inflammation are well established, their function in skin carcinogenesis and host-microbiota interactions remains less understood. Analysis of The Cancer Genome Atlas (TCGA) revealed recurrent mutations in TLR4 in skin cancers, suggesting a potential tumor-suppressive role.

Methods: We used a mouse model with keratinocyte-specific IKKα deletion (Ikka.f/+K5. Cre), with or without TLR4 deficiency. Skin microbial composition was profiled, and 3D skin organoids were generated from murine keratinocytes. These organoids were exposed to tumor-associated bacterial communities to assess DNA damage (γH2AX), IL-1β expression, and lipid metabolism. Comparisons were made with Il4R-/- organoids. In vivo studies included antibiotic treatment and IL-4R signaling ablation.

Results: Ikka.f/+K5.Cre mice showed low tumor incidence, but concurrent TLR4 loss significantly increased squamous cell carcinoma (SCC) formation, with tumors showing loss of the wild-type Ikka allele. Microbiome profiling revealed increased bacterial burden and Firmicutes enrichment in IkkaΔKC/+; Tlr4-/- mice. Organoids exposed to these bacteria showed elevated DNA damage, IL-1β, and altered lipid metabolism responses absent in Il4R-/- organoids. Remarkably, IkkaΔKC/+; Il4R-/- mice were tumor-resistant. Antibiotics also suppressed tumorigenesis.

Conclusion: These findings identify a TLR4–microbiota–IL-4R axis promoting skin cancer in IKKα-deficient epithelium. The 3D organoid model is a valuable platform to study host-microbiota-immune interactions, and IL-4R signaling presents a promising therapeutic target for cancer prevention.

References:

1 Liu B, Xia X, Zhu F, Park E, Carbajal S, Kiguchi K, DiGiovanni J, Fischer SM, Hu Y. IKKα is required to maintain skin homeostasis and prevent skin cancer. Cancer Cell. 2008 Sep 9;14(3):212–225. doi:10.1016/j.ccr.2008.07.015

2 Jariwala N, Leppla SH, Reyes CN, Salao K, de Vera ME, Rollins MR, et al. TLR4 promotes tumor growth and chemoresistance through activation of the β-catenin pathway in skin carcinogenesis. EMBO J. 2010;29(22):3893-904. doi:10.1038/emboj.2010.94.

3 Peralta-Ramos JM, Calcagno ML, Salva MG, Fraccaroli L, De la Fuente AL, Rizzo MM, et al. Toll-like receptor 4 in cutaneous oncology: Dual roles in tumor promotion and suppression. Int J Oncol. 2019;54(6):1981-94. doi:10.3892/ijo.2019.4790.

4 Kobayashi T, Glatz M, Horiuchi K, Kawasaki H, Akiyama H, Kaplan DH, et al. Dysbiosis and oxidative stress in skin carcinogenesis: Emerging concepts and therapeutic implications. Antioxidants (Basel). 2023;12(3):546. doi:10.3390/antiox12030546.

©Matrix Medical Communications. View All Articles.

109—3D organoid modeling reveals how hostmicrobiota interactions fuel skin cancer in the context of TLR4 deficiency and epithelial IKKa reduction
https://jcad.mydigitalpublication.com/articles/109-3d-organoid-modeling-reveals-how-hostmicrobiota-interactions-fuel-skin-cancer-in-the-context-of-tlr4-deficiency-and-epithelial-ikka-reduction

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