Long noncoding RNA CBR3-AS1 mediates tumorigenesis and radiosensitivity of non-small cell lung cancer through redox and DNA repair by CBR3-AS1/miR-409-3p/SOD1 axis

The long noncoding RNA CBR3-AS1 has important functions in various cancers. However, the biological functions of CBR3-AS1 in non-small cell lung cancer (NSCLC) remain unclear. This study aimed to investigate the roles and molecular mechanisms of CBR3-AS1 in NSCLC tumorigenesis and radiosensitivity. Here, we demonstrate CBR3-AS1 overexpression in NSCLC tissue compared with adjacent normal tissue. CBR3-AS1 downregulation reduced proliferation, invasion, and migration; inhibited cell cycle progression; and promoted apoptosis of NSCLC cells. CBR3-AS1 also promoted tumor growth in vivo. CBR3-AS1 may regulate the expression and functions of the miR-409-3p target gene SOD1. CBR3-AS1 expression was negatively correlated with radiosensitivity. CBR3-AS1 downregulation decreased post-irradiation SOD1 expression, increased gamma H2AX formation, raised levels of reactive oxygen species, and promoted apoptosis. Our results suggest that CBR3-AS1 functions as an oncogene through the CBR3-AS1/miR-409-3p/SOD1 pathway, and may represent a new therapeutic target, especially to regulate radiosensitivity in NSCLC.

Automated summary

CBR3-AS1 plays a role in promoting tumorigenesis and reducing radiosensitivity in non-small cell lung cancer, possibly through regulating the miR-409-3p/SOD1 pathway.