Human
head and neck squamous cell carcinoma (
HNSCC) is the sixth most common
cancer type worldwide, possibly due to the significant role of alcohol and tobacco use in its development. Underlying most
cancers are defects in mitochondrial functions such as energy metabolism and apoptosis. In fact, the mutations in
mitochondrial DNA (
mtDNA), which encode
proteins for oxidative phosphorylation (OXPHOS), have been associated with human head and
neck cancers. Here, we investigated the changes in the expression of OXPHOS complexes and the contribution of the defects in mitochondrial translation in the progression of
HNSCC. Western blot analyses of the several stage IVA
HNSCC primary
tumors have shown reduction in the expression of COII and ATP5A of the OXPHOS complexes IV and V subunits, respectively. On the other hand, expression of the majority of the OXPHOS subunits, except complex II SDHB subunit, was impaired in a patient with a stage IV
tumor with a regional lymph node. Interestingly, an overall reduction in one of the mitochondrial-encoded subunits of the complex IV, COII, accentuated a possible defect in mitochondrial translation machinery in two of the stage IVA
tumors. Evidence provided in this study suggests for the first time that the mitochondrial translation defect(s) could be due to a decrease in the expression of one of the essential mitochondrial
ribosomal proteins, MRPL11, in head and neck
tumor biopsies. We also observed an acquired mitochondrial translation deficiency in the HN8 cell line derived from a
lymph node metastasis but not in the HN22 cells derived from the primary
tumor of the same patient. These seminal observations suggest that the mitochondrial translation machinery deserves further investigation for accurate molecular assessment and treatment of
HNSCC.