Overexpression of Thymosin β4 Increases Pseudopodia Formation in LNCaP Prostate Cancer Cells

Abstract

Thymosin β4, a major G-actin-sequestering protein, is known to be involved in tumor metastasis. In the present study, we found that thymosin β4 expression promotes the formation of actin-based pseudopodia-like extensions, associated with cell migration, in human prostate cancer LNCaP cells. Treatment with the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin and Cdc42/Rac1/RhoA inhibitor Clostridium difficile toxin B significantly reduced pseudopodia formation in thymosin β4-overexpressing LNCaP cells, suggesting that the pseudopodia formation by thymosin β4 is probably involved in PI3K and Rho family pathway. We recently reported that thymosin β4 expression is upregulated by androgen deprivation in prostate cancer cells. The increase in thymosin β4 may be one of the causes of prostate cancer progression after androgen ablation therapy.