In vitro effect of Pannexin 1 channel on the invasion and migration of I-10 testicular cancer cells via ERK1/2 signaling pathway.

Pannexin (Panx) plays a crucial role in several cellular processes such as immune cell death, cell proliferation, invasion, and migration, apoptosis, and autophagy. However, the role of Panx in regulating cell migration and invasion in testicular cancer remains to be elucidated. In the present study, we determined the correlation between Panx-1 channel function and migration and invasion in I-10 testicular cancer cells. Transwell and wound healing assays showed that inhibition of Panx-1 by carbenoxolone (CBX) and probenecid (PBN) attenuated the migration and invasion of testicular cancer cells in vitro. Moreover, knockdown of Panx-1 with short hairpin RNA (shRNA) remarkably decreased the migration and invasion ability of I-10 cells. In shRNA-transfected cells, extracellular ATP (released through Panx channel) was also found to be decreased. Similarly, overexpression of Panx-1 with mPanx-1 increased the migration and invasion ability of I-10 cells. Moreover, we found that in mPanx-1-transfected cells treated with U0126 (inhibitor of p-ERK1/2), the migration and invasion of I-10 cells were remarkably attenuated. Overall, increased Panx-1 promotes migration and invasion in testicular cancer cells, and the effect is probably be related with ERK1/2 kinase activity. Thus, Panx-1 can serve as a potential therapeutic target for the treatment of testicular cancer.