Conclusion
Collectively, our research revealed that XRCC2 inhibited the sensitivity of NSCLC to bevacizumab combined with radiotherapy by decreasing cell cycle arrest.
Methods
Gene Expression Profiling Interactive Analysis (GEPIA) database and Starbase database were used to predict the expression level of XRCC2 in NSCLC tissues and the survival time of patients diagnosed with NSCLC, respectively. Besides, qRT-PCR (quantitative real time polymerase chain reaction) and immunoblotting were conducted to confirm the expression of XRCC2 NSCLC tissues and cells. Moreover, cell viability and colony formation were measured by CCK-8 (cell counting kit-8) assay. Cell migration and invasion capabilities were determined by transwell assay. Flow cytometry analysis was employed to detect cell cycle.
Objective
This study aimed to reveal the role and mechanism of X-ray repair cross complementing 2 (XRCC2) and bevacizumab combined with radiotherapy in the treatment of non-small cell lung cancer (NSCLC).
Results
XRCC2 was highly expressed in NSCLC tissues and cells. Additionally, bevacizumab combined with radiotherapy significantly inhibited NSCLC cell proliferation, migration and invasion. Knockdown of XRCC2 further aggravated the role of bevacizumab and radiotherapy in NSCLC, while XRCC2 overexpression reversed these effects efficiently. Furthermore, XRCC2 silence exacerbated the arrest of cell cycle induced by bevacizumab combined with radiotherapy in NSCLC cells, whereas overexpression of XRCC2 alleviated the arrest remarkably.