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.
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.
It has been shown in the present study that global proteomic analysis can produce a set of peptides associated with clinical outcomes for OCSCC.