The Mechanisms of Proliferation and Energy Metabolism in Oral Cancer

Abstract

Human oral squamous cell carcinoma (HOSCC) is the most common head and neck malignant neoplasm. Therapy is generally performed in multidisciplinary approach that used chemotherapy, radiotherapy, and surgery against patients with oral cancer; however, we cannot avoid dysfunction due to its side effects or surgical defects, and it significantly impacts the postoperative quality of life, unfortunately. Therefore, a better understanding of the molecular mechanisms driving oral carcinogenesis may lead to new diagnostic and therapeutic approaches to this disease and improve the prognosis of HOSCC patients. Cancer cells process a fundamental change in its bioenergetics metabolism from normal cells on an altered glucose and lipid metabolism. Recent insights into tumor metabolism have further revealed that oncogenic signaling pathways directly promote metabolic reprogramming to upregulate biosynthesis of lipids, carbohydrates, protein, DNA, and RNA, leading to enhanced growth of tumors. Therefore, targeting cell metabolism has become a novel direction for drug development in oncology. Moreover, molecular mechanisms causing these metabolic changes are just starting to be unraveled. This chapter presents recent findings on molecular markers that have been involved in the mechanisms of proliferation and energy metabolism of oral cancer and in addition provides new perspectives on oral cancer diagnosis and treatments.

Oral Cavity Cancer Tissues Differ in Isotopic Composition Depending on Location and Staging

“…The results were expressed in δ values. For carbon isotopes, we obtained the δ 13 C values by comparing the 13 C/ 12 C ratio in the analysed sample to the isotopic ratio 13 C/ 12 C ratio in the international PDB standard (Pee Dee Bee, Belemnitella Americana). For nitrogen isotopes, we used δ 15 N values related to the 15 N/ 14 N ratio of the standard, which is the atmospheric nitrogen.…”

“…Studies have also confirmed changes in the metabolism of oral cancer cells, revealing that oncogenic signalling pathways directly promote metabolic reprogramming to increase the biosynthesis of lipids, carbohydrates, proteins, DNA, and RNA, leading to increased tumour growth [ 12 ].…”