Exploring the Molecular Mechanisms of Nicotine in Promoting Oral Squamous Cell Carcinoma Progression
Fatima Abdelaziz
Faculty of Science, Assiut University, Egypt
Abstract
Oral squamous cell carcinoma (OSCC) is a prevalent malignancy with a substantial global burden and poor prognosis, particularly in advanced stages. Tobacco smoking and its principal component, nicotine, have been implicated as significant risk factors for OSCC development and progression. This comprehensive research article delves into the intricate molecular mechanisms through which nicotine contributes to the advancement of OSCC. By examining various cellular pathways, signaling cascades, and epigenetic modifications, we aim to elucidate the multifaceted roles of nicotine in promoting tumor growth, invasion, metastasis, and therapeutic resistance. Emphasis is placed on the interplay between nicotine and key oncogenic pathways, such as the PI3K/Akt/mTOR, MAPK, and NF-κB signaling cascades, as well as its effects on epithelial-to-mesenchymal transition (EMT), angiogenesis, and immune evasion. Additionally, the potential involvement of nicotine in modulating the tumor microenvironment and its implications for cancer stem cell maintenance are explored. Through a comprehensive analysis of the current literature and experimental findings, this article provides valuable insights into the molecular underpinnings of nicotine's protumor genic effects in OSCC, paving the way for the development of novel therapeutic strategies and preventive measures.
Author Biography
Fatima Abdelaziz, Faculty of Science, Assiut University, Egypt
