Abstract
Myxoid liposarcoma (MLS) is a mesenchymal malignancy. To identify innovate seeds for clinical applications, we examined the proteomes of primary tumor tissues from 10 patients with MLS with different statuses of postoperative metastasis. The protein expression profiles of tumor tissues were created, and proteins with differential expression associated with postoperative metastasis were identified by two-dimensional difference gel electrophoresis (2D-DIGE) and mass spectrometry. The validation was performed using specific antibodies and in vitro analyses. Using 2D-DIGE, we observed 1726 protein species and identified proteins with unique expression levels in metastatic MLS. We focused on the overexpression of calreticulin in metastatic MLS. The higher expression of calreticulin was confirmed by Western blotting, and gene silencing assays demonstrated that reduced expression of calreticulin inhibited cell growth and invasion. Our findings suggested the important roles of calreticulin in MLS metastasis and supported its potential utility as a prognostic biomarker in MLS. Further investigations of the functional properties of calreticulin and other proteins identified in this study will improve our understanding of the biology of MLS and facilitate novel clinical applications.
Highlights
Myxoid liposarcoma (MLS) is a common type of soft-tissue sarcoma, accounting for approximately one-third of all liposarcomas and 10% of all adult soft-tissue sarcomas [1]
In order to discover the biomarkers to predict the metastasis in patients with MLS, we examined the proteomic profiles of primary tumor tissues from MLS patients with different metastatic statuses
Protein expression profiles of primary tumor tissues were created by 2D-DIGE
Summary
Myxoid liposarcoma (MLS) is a common type of soft-tissue sarcoma, accounting for approximately one-third of all liposarcomas and 10% of all adult soft-tissue sarcomas [1]. Clinical features of MLS are diverse, ranging from localized and curable tumors to metastatic tumors, which can cause tumor-related death. MLS has unique molecular characteristics, including the recurrent translocation t(12:16)(q13:p11) and the corresponding chimeric protein FUS-CHOP (DDIT3, CREBP-homologous protein/DNA damage inducible transcript 3), which is a target of the drug trabectedin [2,3,4,5]. Despite the fact that the unique molecular features are well known in MLS, the origin of MLS remains. Fusion oncoproteins have critical roles in tumor formation, tumor progression is correlated with round cell transformation [6]. The presence of round cells is significantly associated with poor prognosis, and the 5-year survival rates in patients with round cells vary between
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