Abstract
Non‑small‑cell lung cancer (NSCLC) accounts for ~80% of human lung cancers that result in mortalities worldwide. Metastasis‑associated in colon cancer‑1 (MACC‑1) has been demonstrated to be significantly expressed in cases of NSCLC and promotes tumor cell migration and metastasis through transactivation of the metastasis‑inducing hepatocyte growth factor/MET proto‑gene, receptor tyrosine kinase (HGF/MET) signaling pathway. The present study constructed a chimeric antibody (Chanti‑MACC‑1) targeting MACC‑1 and investigated its potential as a molecular therapeutic target in the treatment of NSCLC therapy. The expression of MACC‑1 was detected by reverse transcription‑quantitative polymerase chain reaction and western blotting in lung cancer cell lines and tissues. MTT assay was used to detect proliferation of A549 cells treated by Chanti‑MACC‑1, whereas the functional and regulatory effects of Chanti‑MACC‑1 in the migration and metastasis of NSCLC cells was investigated by a cell invasion assay. The therapeutic effect and survival time was observed in animal models. The results demonstrated that MACC‑1 expression was increased and overexpression of MACC‑1 promoted the progression of the cell cycle, significantly promoted NSCLC cell growth and enhanced tumor migration and invasion through the HGF/MET signaling pathway. It was further demonstrated that Chanti‑MACC‑1 efficiently suppressed MACC‑1 expression and significantly inhibited NSCLC cell proliferation, migration and invasion by blocking the HGF/MET signaling pathway. The data revealed that Chanti‑MACC‑1 was not only beneficial for tumor remission, however additionally contributed to the long‑term survival of NSCLC ‑bearing mice. The findings of the present study indicated that MACC‑1 was significantly upregulated and promoted tumor cell growth and migration in NSCLC cells and tissues via transactivation of the metastasis‑inducing HGF/MET signaling pathway. However, Chanti‑MACC‑1significantly inhibited tumor growth and metastasis, which suggested that MACC‑1 may be essential for tumor initiation and progression by negatively regulating tumor suppressors.