Publication details
Transgelin, an actin associated protein implicated in breast cancer
| Authors | |
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| Year of publication | 2012 |
| Type | Conference abstract |
| MU Faculty or unit | |
| Citation | |
| Description | Transgelin is an abundant protein of smooth muscle cells, which has been widely studied in this cell type. It is associated with F-actin and its function is connected with actin cytoskeleton. Apart from its role in smooth muscles, there emerged an increasing number of studies describing transgelin implication in different types of cancer. However, results of these studies are often contradictory. In our work, we focused on identification of new potential targets of lymph node metastasis in breast cancer. Using 2-D gel electrophoresis we identified transgelin as one of such promising targets. Transgelin was up-regulated in metastatic samples comparing to non-metastatic ones. These results were confirmed at mRNA level using quantitative real-time PCR on a bigger set of samples. Subsequent immunohistochemistry (IHC) further confirmed these expression data. However, based on the results of the IHC staining, it seems, that its up-regulation can be mainly ascribed to stromal not cancer cells. In our further work, we are focusing on transgelin functional characterization in the process of breast cancer metastasis. Using a combination of pull down purification and SILAC metabolic labeling we confirmed transgelin interaction with actin and suggested new potential interaction partners of transgelin. Based on both our expression data, where transgelin has been upregulated in metastatic cancer and its function in F-actin stabilization, we hypothesize its involvement in migration of the cells. Thus, we have studied influence of transgelin silencing on migratory behavior of the cells. Interestingly, we found that transgelin is able both to promote (in BT549 cells) and to inhibit (in PMC42 cells) migration properties of two different breast cancer cell lines. These findings support ambiguous function of transgelin in tumors, which will need further clarification. This work was supported by Czech Science Foundation (project No. P304/10/0868 and by the European Regional Development Fund and the State Budget of the Czech Republic (RECAMO; CZ 1.05/2.1.00/03.0101). Monika Dvorakova is Brno Ph.D. Talent Scholarship Holder – Funded by the Brno City Municipality. |
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