Abstract
Oral squamous cell carcinoma (OSCC) is the 10th most frequent human malignancy and is thus a global burden. Despite some progress in diagnosis and therapy, patients’ overall survival rate, between 40 and 55%, has stagnated over the last four decades. Since the tumor node metastasis (TNM) system is not precise enough to predict the disease outcome, additive factors for diagnosis, prognosis, prediction and therapy resistance are urgently needed for OSCC. One promising candidate is the hypoxia inducible factor-1 (HIF-1), which functions as an early regulator of tumor aggressiveness and is a key promoter of energy adaptation. Other parameters comprise the composition of the tumor microenvironment, which determines the availability of nutrients and oxygen. In our opinion, these general processes are linked in the pathogenesis of OSCC. Based on this assumption, the review will summarize the major features of the HIF system-induced activities, its target proteins and related pathways of nutrient utilization and metabolism that are essential for the initiation, progression and therapeutic stratification of OSCC.
Highlights
Oral squamous cell carcinoma (OSCC) is the 10th most frequent human malignancy worldwide [1,2] with approximately 500,000 new cases each year [3]
The consequences of an increased hypoxia inducible factor 1α (HIF-1α) activity comprise an altered protein expression involved in angiogenesis, metabolic reprogramming, extracellular matrix (ECM) remodeling, epithelial mesenchymal transition (EMT), motility, invasion, metastasis, cancer stem cell maintenance, immune evasion, metabolic adaptations, as well as immunologic changes of the tumor microenvironment (TME) during early carcinogenesis, which have been recently reviewed in detail [3,8,9,10,11,12,13]
We found a correlation between an overexpression of HIF-1α and poorer patients’ survival [15], which was in contrast to a report by Fillies and coauthors [76]
Summary
Oral squamous cell carcinoma (OSCC) is the 10th most frequent human malignancy worldwide [1,2] with approximately 500,000 new cases each year [3]. During the last 20 years, the molecular, metabolic and immunologic features of this disease have been well characterized These include some essential hallmarks in cancer development, such as sustained proliferation, evasion from growth suppressors, resistance to cell death, replicative immortality, enhanced angiogenesis, increased invasion and metastasis, as well as alterations in the cellular metabolism [4,5]. This minireview will address the possibilities of OSCC to adapt for enhanced growth, tumor progression and metastasis formation with the focus on the role of metabolic changes in these processes
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