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Jin, Lin; Kashyap, Mahendra P.; Chen, Yunjia; Khan, Jasim; Guo, Yuanyuan; Chen, Jari Q.; Lee, Madison B.; Weng, Zhiping; Oak, Allen; Patcha, Prasanth; Mayo, Tiffany; Sinha, Rajesh; Atigadda, Venkatram; Mukhtar, Shahid M.; Deshane, Jessy S.; Raman, Chander; Elston, Carly; Elewski, Boni E.; Elmets, Craig A.; Athar, Mohammad
iScience, 06/2023, Letnik: 26, Številka: 6Journal Article
Hidradenitis suppurativa (HS) is a skin disorder that causes chronic painful inflammation and hyperproliferation, often with the comorbidity of invasive keratoacanthoma (KA). Our research, employing high-resolution immunofluorescence and data science approaches together with confirmatory molecular analysis, has identified that the 5′-cap-dependent protein translation regulatory complex eIF4F is a key factor in the development of HS and is responsible for regulating follicular hyperproliferation. Specifically, eIF4F translational targets, Cyclin D1 and c-MYC, orchestrate the development of HS-associated KA. Although eIF4F and p-eIF4E are contiguous throughout HS lesions, Cyclin D1 and c-MYC have unique spatial localization and functions. The keratin-filled crater of KA is formed by nuclear c-MYC-induced differentiation of epithelial cells, whereas the co-localization of c-MYC and Cyclin D1 provides oncogenic transformation by activating RAS, PI3K, and ERK pathways. In sum, we have revealed a novel mechanism underlying HS pathogenesis of follicular hyperproliferation and the development of HS-associated invasive KA. Display omitted •eIF4F is associated with follicular hyperproliferation in HS•eIF4F targets Cyclin D1 and c-MYC are highly expressed activating Ras, PI3K, and ERK•The interplay of Cyclin D1 and c-MYC is associated with HS-related KA pathogenesis•nCyclin D1-CDK4 expressed throughout KA lesions providing oncogenic signaling Biological sciences; Biochemistry; Medical biochemistry
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in: SICRIS
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