Abstract
Considering the great energy and biomass demand for cell survival, cancer cells exhibit unique metabolic signatures compared to normal cells. Head and neck squamous cell carcinoma (HNSCC) is one of the most prevalent neoplasms worldwide. Recent findings have shown that environmental challenges, as well as intrinsic metabolic manipulations, could modulate HNSCC experimentally and serve as clinic prognostic indicators, suggesting that a better understanding of dynamic metabolic changes during HNSCC development could be of great benefit for developing adjuvant anti-cancer schemes other than conventional therapies. However, the following questions are still poorly understood: (i) how does metabolic reprogramming occur during HNSCC development? (ii) how does the tumorous milieu contribute to HNSCC tumourigenesis? and (iii) at the molecular level, how do various metabolic cues interact with each other to control the oncogenicity and therapeutic sensitivity of HNSCC? In this review article, the regulatory roles of different metabolic pathways in HNSCC and its microenvironment in controlling the malignancy are therefore discussed in the hope of providing a systemic overview regarding what we knew and how cancer metabolism could be translated for the development of anti-cancer therapeutic reagents.
Highlights
Malignancies of the head and neck influence a variety of anatomic sites, including the oral cavity, oropharynx, nasopharynx, hypopharynx, larynx, and salivary glands [1]
Cellular retinoic acid binding protein (CRABP) expression was enriched in tumor tissues compared with its adjacent normal tissues [22], while additional studies confirmed that external retinoic acid administration could modulate the Epidermal Growth Factor Receptor (EGFR) activity, a key predisposition of Head and Neck Squamous Cell Carcinomas (HNSCC) development [23]
These findings suggest that methionine could be tumor-suppressive and that the methionine content might serve as a prognostic factor for HNSCC patients, one must still mechanistically clarify the way in which methionine regulates epigenetic modification in HNSCC development
Summary
Malignancies of the head and neck influence a variety of anatomic sites, including the oral cavity, oropharynx, nasopharynx, hypopharynx, larynx, and salivary glands [1]. While cancer metabolism is receiving increasing attention [19,20], most studies were conducted to target a single metabolic enzyme or metabolite in controlling tumorigenesis, without analyzing global metabolic alterations. In this way, to escape death, cancer cells could possibly evolve and develop alternative compensatory metabolic changes [21]. Systemic manipulations to direct the tumor cell metabolic status “back” to the normal cell status, thereby lessening the cancer malignancy, is desired (Figure 1B). The goal of the review is to provide a systemic overview regarding the current understanding of cancer metabolism and its clinical potential, with an emphasis on HNSCCs
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