Abstract:
Objective To investigate the diagnostic value and mechanism of carbonic anhydrase 1(CA1) in the early stage of non-small cell lung cancer (NSCLC).
Methods Serum CA1 levels in patients with early stage NSCLC were determined by ELISA.In vitro (in A549, H520, and H1299 cells), we used RNA interference to knock down the expression of CA1 and used plasmid transfection to establish a CA1 over-expression model.A CCK-8 assay was used to detect cell proliferation in different treatment groups.Real-time quantitative polymerase chain reaction (PCR) and Western blot were used to detect the mRNA and protein expression levels of Wnt3a and β- catenin, which are the key components in the Wnt/β-catenin signaling pathway.
Results The expression of CA1 in the serum of patients with early NSCLC was significantly higher than that in healthy individuals.After knocking down the expression of CA1 by sh-RNA, the proliferation rates of A549, H520, and H1299 were significantly reduced, while after overexpression of CA1, the cell proliferation rate increased.CA1 can also effectively regulate the expression levels of Wnt3a and β-catenin in the Wnt/β-catenin signaling pathway.
Conclusions CA1 may affect the proliferation of NSCLC through the Wnt/β-catenin signaling pathway, especially by Wnt3a and β- catenin; CA1 is expected to become a new biomolecular marker for the early diagnosis of NSCLC.