Source: 7thspace.com
Author: staff

Oral squamous cell carcinoma (OSCC) is one of the most common forms of cancer associated with the presence of precancerous oral leukoplakia. Given the poor prognosis associated with oral leukoplakia, and the difficulties in distinguishing it with cancer lesion, there is an urgent need to elucidate the molecular determinants and key signal pathways underlying the malignant transformation of precancerous to cancerous tissue, and thus to identify novel diagnostic and therapeutic target.

Results:
We have utilized two dimensional electrophoresis followed by ESI-Q-TOF-LC-MS/MS to identify proteins differentially expressed in six pairs of oral leukoplakia tissues with dysplasia and oral squamous cancer tissues, each pair from the same patient.

Approximately 85 differentially and constantly expressed proteins (>two-fold change, P>0.05) were identified, 52 up-regulated and 33 down-regulated. Gene ontological methods were employed to identify the biological processes that were over-represented in this carcinogenic stage.

Potential biological networks were also constructed to reveal the link between those protein candidates. Among those proteins, three homologs of proteosome activator PA28 a,b and g were shown to have up-regulated mRNA levels in OSCC cells relative to oral keratinocytes.

Conclusions:
Amounts of differentially expressed proteins involved in the malignant transformation of oral leukoplakia.

Their expression level, bioprocess, interactions networks could be analyzed by bioinformatics approach. All the three homologs of PA28 may be shown to play an important role in the malignant transformation.

Our study is an example of a systems biology study, in which functional proteomics was constructed to help to elucidate mechanistic aspects and potential involvement of proteins. Our results may provide new insights into the pathogenesis of oral cancer.

These differentially expressed proteins may have utility as useful candidate markers of OSCC.

Source:
BMC Genomics 2009, 10:383

Authors:
Wang Zhi, Feng Xiaodong, Liu Xinyu, Jiang Lu, Zeng Xin, Ji Ning, Li Jing, Li Longjiang, Chen Qianming