CXCL13 Activates Akt to Promote Radioresistance of Lung Cancer

Abstract

Objective To investigate the role and molecular mechanism of CXCL13 on the radioresistance of lung cancer. Methods Public database was used to analyze the expression levels of CXCL13 and CXCR5 in lung cancer patients, and the relation between the expression levels of CXCL13/CXCR5 and the prognosis of lung cancer patients who received radiotherapy only. Western blot was used to detect the effects of different concentrations of CXCL13 and Akt inhibitor LY294002 on Akt expression and activation in human lung cancer H1975 cells. CCK-8 method, flow cytometry and clone formation assay were used to analyze the effect of CXCL13 and LY294002 on the proliferation, apoptosis and cell clone formation ability after X ray radiation treatment, respectively. Results The expression levels of CXCL13 and its receptor CXCR5 in lung cancer patients were significantly higher than those in the normal group (P < 0.003). The high expression level of CXCL13 is closely related to the progression of postnatal survival (PPS) of lung cancer patients. H1975 cells treated with 100ng/ml CXCL13 showed significantly higher proliferation level (P=0.015) and clone formation ability (P=0.014), but lower apoptosis level (P=0.001) than the control group. 100ng/ml CXCL13 significantly activated Akt. After 8Gy X-ray radiation treatment, the cell proliferation level (P=0.019) and clone formation ability (P=0.001) in the 20μg/ml LY294002 combined with CXCL13 group were significantly lower than those in the CXCL13 group alone, while the apoptosis level in the combination group was significantly higher than that in the CXCL13 group alone (P=0.003). Conclusion CXCL13 promotes the radioresistance of lung cancer by activating Akt.

Keywords

• cxcl13
• akt
• radioresistance
• lung cancer