Inflammatory response or oxidative stress induces upregulation of PTPN2 and thus promotes the progression of laryngocarcinoma.

OBJECTIVE

This study aims to investigate whether inflammatory response or oxidative stress could induce upregulation of PTPN2, thus promoting the progression of laryngocarcinoma.

PATIENTS AND METHODS

PTPN2 levels in laryngocarcinoma tissues and normal tissues were detected. In addition, PTPN2 levels in laryngocarcinoma tissues with stage 1/2 or stage 3/4 were determined as well. In vitro abundance of PTPN2 was measured in laryngocarcinoma cells and immortalized human nasopharyngeal epithelial cells. Survival analysis was conducted in laryngocarcinoma patients with high or low expression level of PTPN2. Subsequently, M4E cells were stimulated with inflammation (IFN-γ or TNF-α treatment) or oxidative stress (H2O2 stimulation), followed by determination of the protein level of PTPN2. In M4E cells stimulated with different concentrations of H2O2, the clonality and Ki-67 positive cell ratio were detected. Finally, clonality and Ki-67 positive cell ratio in M4E cells transfected with negative control or sh-PTPN2, regardless of H2O2 stimulation, were assessed.

RESULTS

PTPN2 was upregulated in laryngocarcinoma tissues, especially those in stage 3/4. Similarly, in vitro abundance of PTPN2 was higher in laryngocarcinoma cell lines. The high level of PTPN2 predicted poor prognosis in laryngocarcinoma patients. IFN-γ or TNF-α treatment upregulated the protein level of PTPN2. Meanwhile, H2O2 stimulation upregulated the protein level of PTPN2, dose-dependently increased clonality, and Ki-67 positive cell ratio in M4E cells. The knockdown of PTPN2 suppressed clonality and Ki-67 positive cell ratio in M4E cells stimulated by H2O2 or not.

CONCLUSIONS

Inflammatory response or oxidative stress could induce upregulation of PTPN2, thus promoting the proliferative ability of laryngocarcinoma.