As part of our initial screen for candidate proteins with possible clinical relevance, we restricted our analyses to a subset (n = 28) of OCSCC patients for whom we had at least 2 years of clinical follow-up, and assessed differences in peptide levels isolated from the 6 salt cuts between patients with and without evidence of disease progression within 2 years of diagnosis.
Twenty eight OCSCC specimens for which we had at least 24 months of clinical follow-up data were tested for 3 outcomes; disease-specific death (DSD), DM, and loco regional recurrence.
For the current study we limited the analysis to a single clinical outcome, DM, to focus on studying OCSCC's predilection to early DM.
We did not observe a strong relationship between DSP expression and DNA methylation in our cohort (data not shown), which suggests an alternative mechanism of silencing in OCSCC. They went on to demonstrate that overexpression of DSP led to increased plakoglobin ([gamma]-catenin).
(45) This observation with our study suggests that suppressed TRIM29 may promote AIG, contributing to poorer outcome in OCSCC.
In the case of TRIM 29, its reduction was associated with poorer prognosis, even though it can function as both an oncogenic protein and a tumor suppressor, (49) possibly because of the state of p53, that is, posttranslational modification and/or mutation, directly involved in the OCSCC tumorigenesis.
However, that is not meant to imply that proteins with weaker correlations to their mRNAs lack importance in OCSCC progression.