PMID- 28944826 OWN - NLM STAT- MEDLINE DCOM- 20180606 LR - 20231124 IS - 1791-3004 (Electronic) IS - 1791-2997 (Print) IS - 1791-2997 (Linking) VI - 16 IP - 5 DP - 2017 Nov TI - MACC‑1 antibody target therapy suppresses growth and migration of non‑small cell lung cancer. PG - 7329-7336 LID - 10.3892/mmr.2017.7517 [doi] AB - 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. FAU - Shi, Woda AU - Shi W AD - Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China. FAU - Song, Jianxiang AU - Song J AD - Department of Cardiothoracic Surgery, The Third People's Hospital, Yancheng, Jiangsu 224001, P.R. China. FAU - Wang, Wencai AU - Wang W AD - Department of Cardiothoracic Surgery, The Third People's Hospital, Yancheng, Jiangsu 224001, P.R. China. FAU - Zhang, Yajun AU - Zhang Y AD - Department of Cardiothoracic Surgery, The Third People's Hospital, Yancheng, Jiangsu 224001, P.R. China. FAU - Zheng, Shiying AU - Zheng S AD - Department of Cardiothoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China. LA - eng PT - Journal Article PT - Retracted Publication DEP - 20170919 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (Antibodies, Monoclonal) RN - 0 (MACC1 protein, human) RN - 0 (Recombinant Fusion Proteins) RN - 0 (Trans-Activators) RN - 0 (Transcription Factors) RN - 67256-21-7 (Hepatocyte Growth Factor) RN - EC 2.7.10.1 (Proto-Oncogene Proteins c-met) SB - IM RIN - Mol Med Rep. 2024 Jan;29(1):. PMID: 37997799 MH - A549 Cells MH - Animals MH - Antibodies, Monoclonal/genetics/metabolism/*pharmacology/therapeutic use MH - Carcinoma, Non-Small-Cell Lung/drug therapy/metabolism/*pathology MH - Cell Line, Tumor MH - Cell Movement/drug effects MH - Cell Proliferation/*drug effects MH - Down-Regulation/drug effects MH - Epithelial-Mesenchymal Transition/drug effects MH - Female MH - Hepatocyte Growth Factor/metabolism MH - Humans MH - Lung Neoplasms/drug therapy/metabolism/*pathology MH - Mice MH - Mice, Inbred C57BL MH - Microscopy, Fluorescence MH - Proto-Oncogene Proteins c-met/metabolism MH - Recombinant Fusion Proteins/biosynthesis/genetics/pharmacology/therapeutic use MH - Signal Transduction/drug effects MH - Trans-Activators MH - Transcription Factors/genetics/*immunology/metabolism MH - Transplantation, Heterologous PMC - PMC5865862 EDAT- 2017/09/26 06:00 MHDA- 2018/06/07 06:00 PMCR- 2017/09/19 CRDT- 2017/09/26 06:00 PHST- 2016/04/04 00:00 [received] PHST- 2017/08/14 00:00 [accepted] PHST- 2017/09/26 06:00 [pubmed] PHST- 2018/06/07 06:00 [medline] PHST- 2017/09/26 06:00 [entrez] PHST- 2017/09/19 00:00 [pmc-release] AID - mmr-16-05-7329 [pii] AID - 10.3892/mmr.2017.7517 [doi] PST - ppublish SO - Mol Med Rep. 2017 Nov;16(5):7329-7336. doi: 10.3892/mmr.2017.7517. Epub 2017 Sep 19.