Abstract
Adenoid cystic carcinoma (ACC) is an extremely rare salivary gland tumor with a poor prognosis and needs attention on molecular mechanisms. Protein ubiquitination is an evolutionarily conserved post-translational modification (PTM) for substrates degradation and controls diverse cellular functions. The broad cellular function of ubiquitination network holds great promise to detect potential targets and identify respective receptors. Novel technologies are discovered for in-depth research and characterization of the precise and dynamic regulation of ubiquitylomics in multiple cellular processes during cancer initiation, progression and treatment. In the present study, 4D label-free quantitative techniques of ubiquitination proteomics were used and we identified a total of 4152 ubiquitination sites in 1993 proteins. We also performed a systematic bioinformatics analysis for differential modified proteins and peptides containing quantitative information through the comparation between oral ACC (OACC) tumor with adjacent normal tissues, as well as the identification of eight protein clusters with motif analysis. Our findings offered an important reference of potential biomarkers and effective therapeutic targets for ACC.
Highlights
Adenoid cystic carcinoma (ACC) was discovered a long time ago with location in the major and minor salivary glands [1,2] and other organs [3], which can be divided into tubular form (Grade I), cribriform (Grade II) and solid form (Grade III) [4]
In order to globally reveal the involvement of ubiquitin in the progression and regulation of oral ACC (OACC), we performed 4D label-free quantitative ubiquitination proteomics study through comparing OACC tumor samples (OACC T) with the adjacent normal samples (OACC N) in four patients who had not received any drug treatment before operation
OACC T showed 555 ubiquitination sites up-regulated (≥1.5-fold, P-value
Summary
Adenoid cystic carcinoma (ACC) was discovered a long time ago with location in the major and minor salivary glands [1,2] and other organs [3], which can be divided into tubular form (Grade I), cribriform (Grade II) and solid form (Grade III) [4]. Several factors have been studied to associate with the clinicopathological parameters and prognosis of ACC, including p53 [8], SOX2 [9], mutated ATM [10], MACC1 [11], WHSC1 [12], EpCAM [13], PSMA [14], TRAF6 [15], HSP27 [16], PRRX1 [17], hypoxia-related genes [18], the EGFR pathway genes [19], MYB–NFIB fusion genes [20,21,22,23], as well as NOTCH1-HEY1 pathway [24] and Akt signaling pathway [25,26]. Considering the aggressive behavior, it is urgent to figure out more efficient clinical pathological and biomolecular prognostic factors for therapeutic choices
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