Transgelin is a protein reported to be a marker of several cancers. However, previous studies have shown both up- and down-regulation of transgelin in tumors when compared with non-tumor tissues and the mechanisms whereby transgelin may affect the development of cancer remain largely unknown. Transgelin is especially abundant in smooth muscle cells and is associated with actin stress fibers. These contractile structures participate in cell motility, adhesion, and the maintenance of cell morphology. Here, we focused on the role of transgelin in breast cancer. Initially, we studied the effects of transgelin on cell migration using the breast cancer cell lines, BT 549 and PMC 42. Using the xCELLigence system, we found opposite results in the two cell lines. Transgelin silencing increased the migration of PMC 42 cells, but decreased the migration of BT 549 cells. To further clarify these contradictory results, we performed an experiment to quantify the changes in protein expression after transgelin silencing in these two cell lines, using quantitative proteomics (iTRAQ-2DLC-MS/MS). Our results confirmed the role of transgelin in the migration of BT 549 cells and suggested the involvement of transgelin in apoptosis and small molecule biochemistry in PMC 42 cells. The context-dependent function of transgelin reflects the different molecular backgrounds of these cell lines, which differ in karyotypes, mutation statuses, and proteome profiles. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.