There still have some studies which were concerning of aberrant overexpression of vimentin and its relationship with melanoma metastasis [28, 29]. On the whole, we first demonstrated the significant upregulation of vimentin in metastatic melanoma compared to primary cases by proteomics and carried
out the clinical verification to evalute whether vimentin is a potential biomarker for predicting the metastasis in melanoma patients. Vimentin see more is one of the most familiar members of intermediate filaments (IFs) which is the characteristic of mesenchymal cells. IFs, actin microfilaments and microtubules are three major structural components of the cytoskeleton which are in charge of contraction and migration of cells. In addition, the stucture where vimentin, actin associate with integrins and where vinculin and plectin recruited were termed as the vimentin associated matrix adhesions (VAMs) [30]. Of our results, laminin
receptor and actin (β,γ) were all up-regulation in the metastatic group. It revealed that cytoskeleton proteins might be associated with melanoma metastasis intensively. Metastasis is a complicated process, of them adhesion is a prerequisite step by which tumor cells could be easy to migrate, invade and detach from the R788 clinical trial primary tumour. Recent studies have revealed that vimentin has key roles in adhesion by regulating integrin functions [31]. So it could be as a therapeutic target for melanoma in the future. In addition to this, Vimentin is still the predominant mesenchymal marker which is atypical expressed in the epithelial-mesenchymal transition (EMT). EMT is the process that the epithelial cells acquire the mesenchymal phenotype with more
migratory and invasive properties. Resently, more and more attentions have been focused on the EMT which seems to act as a switch for the initial cancer metastasis[32]. Generally, EMT is defined as the tuclazepam upregulation of mesenchymal markers and downregulation of epithelial markers. Till now, there have been some reports to identify that melanoma metastasis were associated with EMT [33, 34]. Alonso et al [34] confirmed that the expression of a set of proteins included in the EMT group (N-cadherin, osteopontin, and SPARC/osteonectin) were significantly associated with metastatic development of melanomas using cDNA microarrays. In our MS results, only vimentin and actin were identified up-regulated, no other epithelial markers were identified, that is one shortcoming of our study. So it is merely a hypothesis that vimentin involving in the melanoma metastasis is by EMT progression. Conclusions This is the first report to validate the proteomics results in a set of melanoma samples. Our results showed that increased expression of vimentin might be as a novel metastatic indicator for melanoma. In other words, vimentin is not only the dignostic marker but also the hematogenous metastasis predictor for melanomas clinically.