Journal
CELLS
Volume 10, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/cells10030606
Keywords
squamous cell carcinoma; metabolism; oxidative stress
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Squamous cell carcinomas (SCCs) are common solid tumors that have not fully benefited from recent advances in molecularly targeted therapy or immunotherapy. A lack of a consolidated perspective on genetic aberrations and essential factors for SCC pathogenesis, as well as cellular heterogeneity in SCC, has contributed to a critical dearth in effective and specific therapies. Emerging evidence characterizing the distinct genomic, epigenetic, and metabolic landscapes of SCC may reveal targetable vulnerabilities at their intersection.
Squamous cell carcinomas (SCCs) arise from both stratified squamous and non-squamous epithelium of diverse anatomical sites and collectively represent one of the most frequent solid tumors, accounting for more than one million cancer deaths annually. Despite this prevalence, SCC patients have not fully benefited from recent advances in molecularly targeted therapy or immunotherapy. Rather, decades old platinum-based or radiation regimens retaining limited specificity to the unique characteristics of SCC remain first-line treatment options. Historically, a lack of a consolidated perspective on genetic aberrations driving oncogenic transformation and other such factors essential for SCC pathogenesis and intrinsic confounding cellular heterogeneity in SCC have contributed to a critical dearth in effective and specific therapies. However, emerging evidence characterizing the distinct genomic, epigenetic, and metabolic landscapes of SCC may be elucidating unifying features in a seemingly heterogeneous disease. In this review, by describing distinct metabolic alterations and genetic drivers of SCC revealed by recent studies, we aim to establish a conceptual framework for a previously unappreciated network of oncogenic signaling, redox perturbation, and metabolic reprogramming that may reveal targetable vulnerabilities at their intersection.
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