Abstract
The non-receptor protein tyrosine phosphatase 23 (PTPN23) has been reported to inhibit cancer cell migration and invasion and is involved in the endocytosis process. However, the mechanisms of PTPN23 in blocking tumorgenesis remain unclear. Here, we used lung cancer cell line H1299 as a cell model to elucidate the role of phosphatase PTPN23 in lung cancer. We found that PTPN23 can enhance tumor necrosis factor (TNF)-induced apoptosis. Moreover, PTPN23 also decrease the phosphorylation of epidermal growth factor receptor (EGFR) and ERK1/2 induced by EGF. According to previous data, we suggest PTPN23 is involved the down-regulation of receptor, although our immunofluorescence data show that lose of PTPN23 does not affect receptor internalization. However, lung cancer cells with mutant EGFR showed lower levels of PTPN23 than those with wild type EGFR. Decreasing PTPN23 expression was also observed in lung cancer developed in EGFR mutant-transgenic mice. The collective data suggest that PTPN23 may serve as a tumor suppressor in lung cancer through modulating EGFR and TNFR signaling pathways.