@Article{biocell.2026.082448,
AUTHOR = {Bianca Voicu Balasea, Alexandra Popa, Florentina Rus, Radu Radulescu, Melis Izet, Alexandra Ripszky},
TITLE = {Implications of KRAS in Molecular Signaling Pathways in Oral Squamous Cell Carcinoma: Interplay with Autophagy, Apoptosis, and Oxidative Stress},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27014},
ISSN = {1667-5746},
ABSTRACT = {Oral squamous cell carcinoma (OSCC) is an aggressive malignancy often diagnosed at advanced stages and associated with poor prognosis. This review aims to summarize the role of Kirsten rat sarcoma viral oncogene homolog (KRAS) signaling in OSCC progression, with particular emphasis on its involvement in the regulation of autophagy, apoptosis, and oxidative stress. KRAS contributes to tumor progression despite the low frequency of activating mutations, primarily through increased KRAS expression associated with activation of downstream signaling pathways, including phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) and rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (RAF/MEK/ERK). Collectively, KRAS is involved in a complex regulatory network comprising apoptosis, autophagy, and oxidative stress, thereby influencing tumor cell survival and therapeutic resistance. Targeting these pathways may represent a promising strategy to restore apoptotic responses and overcome treatment resistance in OSCC.},
DOI = {10.32604/biocell.2026.082448}
}