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- W4285992587 abstract "Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer. Emerging evidence suggests that homeoproteins can act as modulators of tumor initiation and progression in cSCC. DLX3 is a homeobox transcription factor which plays pivotal roles in embryonic development and epidermal homeostasis. Previous work from our lab, using both human samples and a Dlx3 knock-out (Dlx3cKO) mouse model, demonstrated DLX3’s tumor suppressive role in epithelial tumor development and tumor progression. Molecular evaluation of the Dlx3cKO tumor-permissive properties identified specific mechanisms of Dlx3-mediated skin carcinogenesis via upregulation of EGFR ligands and activation of EGFR/ERBB2/MAPK pathway. Here, we have investigated the direct DLX3 genomic targets and signal pathways mediating DLX3’s tumor suppressive function. Epigenetic studies using chromatin immunoprecipitation (ChIP) and next-generation DNA sequencing demonstrated that DLX3 is directly recruited into the regulatory regions of EGFR ligand genes including Areg, Ereg, Tgfα and Btc. Further, transcriptomic profiling using RNA sequencing identified STAT3 as a downstream mediator of EGFR/ERBB2 pathway activation in Dlx3cKO skin. Thus, our preliminary results support that STAT3 is a key downstream modulator of DLX3’s tumor suppressive activity in cSCC. Future work will functionally evaluate the in-silico findings to elucidate the downstream events critical to gene activation important in skin tumorigenesis." @default.
- W4285992587 created "2022-07-21" @default.
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- W4285992587 date "2022-08-01" @default.
- W4285992587 modified "2023-09-28" @default.
- W4285992587 title "088 Deciphering the molecular signals of EGFR pathway activation in Dlx3 deficient skin in cSCC" @default.
- W4285992587 doi "https://doi.org/10.1016/j.jid.2022.05.023" @default.
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