Background: Non-small cell lung cancer (NSCLC) seriously endangers human health. Circular RNAs (circRNAs) regulate diverse types of cancers, including NSCLC. This study investigated the possible mechanism of circ0001313  in NSCLC.
Materials and Methods: Circ0001313  expression in NSCLC tissues was measured, and its correlation with clinicopathological features was analyzed. The binding relationships among circ0001313 , microRNA (miR)-452 and HMGB3  were tested. The gain and loss of functions were performed to examine NSCLC cell malignant behaviors. After HMGB3  overexpression, ERK/MAPK pathway-related protein levels were detected. Subsequently, the rescue experiment was further performed using an ERK/MAPK pathway inhibitor PD98059.
Results: Abnormally elevated circ0001313  and decreased miR-452  in NSCLC cells were observed. Circ0001313  silencing or miR-452  overexpression significantly reduced NSCLC cell proliferation and invasion. Circ0001313  competitively bound to miR-452  to upregulate HMGB3 , thus promoting NSCLC cell growth. HMGB3  overexpression activated the ERK/MAPK pathway to contribute to NSCLC development.
Conclusion: We highlighted that silencing of circ0001313  blunted the ERK/MAPK pathway via the miR-452/HMGB3  axis, thereby inhibiting NSCLC cell proliferation and invasion.
Keywords: non-small cell lung cancer, circular RNA 0001313, microRNA-452, HMGB3 , ERK/MAPK pathway, proliferation and invasion