Inhibition of TrxR2 suppressed NSCLC cell proliferation, metabolism and induced cell apoptosis through decreasing antioxidant activity

- TrxR2 was up-regulated in lung cancer tissues.
- Inhibition of TrxR2 inhibited cell proliferation, metabolism and induced apoptosis.
- Inhibition of TrxR2 induced ROS production and decreased antioxidant activity.
- TrxR2 acts as an oncogenic gene in the context of lung cancer progression.

AimsThis study aims to analyze the effect of thioredoxin reductase 2 (TrxR2) on lung cancer cell proliferation, apoptosis, invasion and migration in vitro.Main methodsReal-time PCR was used to measure the expression of TrxR2 in NSCLC tumor tissues. After pAd-TrxR2 or shRNA-TrxR2 was transfected into A549 or NCI-H1299 cells, the cell proliferation was measured by CCK-8 method; cell apoptosis was measured by flow cytometry; cell invasion and migration was measured by Transwell method. The production of ROS was measured by DCFH-DA method; the activity of SOD, CAT and GSH-Px was measured by relative ELISA kit.Key findingsThe results showed that TrxR2 was up-regulated in NSCLC tumor tissues. Inhibition of TrxR2 suppressed NSCLC cell proliferation and induced apoptosis, and inhibited cell invasion and migration. However, overexpression of TrxR2 showed the opposite effect. Furthermore, when cells were transfected with shRNA-TrxR2, the production of ROS was significantly increased, and SOD, CAT and GSH-Px activity was decreased. Conversely, pAd-TrxR2 transfection showed the opposite effect.SignificanceTaken together, our results suggest that TrxR2 acts as an oncogenic gene in the context of lung cancer progression. The inhibition of TrxR2 suppressed lung cancer cell proliferation, invasion and migration and induced cell apoptosis by inducing ROS production and decreasing antioxidant activity. TrxR2 may be a potential target for NSCLC treatment.