Cortex Mori extract inhibits migration and invasion of lung adenocarcinoma cells by blocking RECQL4-induced NF-κB and ERK signaling pathways

Lung adenocarcinoma (LUAC) is one of the usual tumors of the lung with high mortality rate. RecQ-like helicase 4 (RECQL4) gene has been discovered to take part in the progression of different cancers by undertaking as an oncogene, and is relevant with poor prognosis of LUAC. Cortex Mori (CM) extract has been investigated to affect cellular progress to regulate different diseases. However, the detailed functioning of RECQL4 and CM extract, as well as their regulatory mechanisms in LUAC, has not been illustrated. The purpose of the present study was to probe the impact of RECQL4 and CM extract on progression of LUAC. The expression of RECQL4 in LUAC was assessed by The Cancer Genome Atlas (TCGA) database. The mRNA expression of RECQL4 was examined by real-time quantitative polymerase chain reaction. The protein expressions (epithelial–mesenchymal transition [EMT] process, nuclear factor kappa B [NF-κB] and extracellular signal-regulated kinase [ERK] signaling pathways-related proteins) were determined by Western blot analysis. The cell proliferation was tested through cell counting kit-8 assay. Cell migration and invasion was affirmed by wound-healing and transwell assays. The cell senescence was assessed through senescence-associated beta-galactosidase staining. The cell cycle was inspected by flow cytometry. Our findings demonstrated that RECQL4 exhibited higher expression in LUAC tissues and cell lines. Through functional experiments, we found that RECQL4 facilitated cell proliferation, migration, and invasion as well as EMT progression. In addition, RECQL4 relieved cell cycle arrest and cell senescence. Moreover, RECQL4 activated NF-κB and ERK signaling pathways by enhancing phospho(p)-p65–p65 and p-ERK–ERK levels in LUAC. CM extract exhibited antitumor effects in LUAC, and blocked RECQL4-induced NF-κB and ERK signaling pathways. Our results manifested that CM extract inhibited migration and invasion of LUAC cells by blocking RECQL4-induced NF-κB and ERK signaling pathways. This result could provide a promising therapeutic strategy for LUAC.