Flacco, NiclaEstornut Navarro, CristinaRoger Laparra, InésRibera, PilarSánchez Herrera, GermánTrujillo Barberá, SilviaPérez Leal, Martín2026-05-022026-05-022026Flacco, N., Estornut, C., Roger, I., Ribera, P., Sánchez-Herrera, G., Trujillo-Barbera, S., & Pérez-Leal, M. (2026). PI3K/mTOR inhibition attenuates cigarette smoke-induced senescence and SASP in oral fibroblasts: Implications for tumor microenvironment remodeling. Frontiers in Cell and Developmental Biology, 14, 1745944. https://doi.org/10.3389/fcell.2026.17459442296-634Xhttps://hdl.handle.net/11268/17064Cigarette smoke exposure is a major risk factor for oral cancer, partly due to its ability to induce early molecular alterations in the oral mucosa. Cellular senescence and the senescence-associated secretory phenotype (SASP) contribute to chronic inflammation and microenvironmental remodeling, favoring carcinogenesis. The PI3K/AKT/mTOR pathway has been implicated in sustaining SASP and senescence, suggesting that its inhibition may represent a promising preventive strategy.engAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/BiocienciasFibroblastosFenotipo secretor asociado a la senescenciaMicroambiente tumoraljournal article10.3389/fcell.2026.1745944open accessTabaquismoInvestigación médicaMedicina preventivaGoal 3: Ensure healthy lives and promote well-being for all at all ages