PI3K/mTOR inhibition attenuates cigarette smoke-induced senescence and SASP in oral fibroblasts: implications for tumor microenvironment remodeling

Abstract

Cigarette 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.