To test the hypothesis that overexpression of this G-actin sequestering peptide also promotes tumor invasion, we examined not only the invasion capability of Tbeta-4-overexpressing SW480 cells, but also the expression levels of Tbeta-4 as well as several proteins that participate in different stages of tumor progression in matched samples of human primary colorectal adenocarcinoma and liver metastases from several patients.
On the basis of these data, the process of epithelial-mesenchymal transition could represent the unifying process that explains the role of Tβ4 during fetal development and in cancer progression.
In conclusion, the TGFβ/Tβ4/MRTF/SRF pathway is critical for metastasis and tumor progression.<b>Implications:</b> These findings define a molecular mechanism underlying a tumor-promoting function of thymosin β4 through activation of MRTF/SRF signaling.<i></i>.
The genes for PFN1 and TMSB4 are both highly expressed in oral tissue and both encode actin monomer binding proteins thought to play a role in cell motility and possibly other crucial parts of tumor progression.