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

Qin Li, Enyao Wei, Wenbin Zhang, Feng Zhang
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Abstract

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.
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桑皮质提取物通过阻断recql4诱导的NF-κB和ERK信号通路抑制肺腺癌细胞的迁移和侵袭
肺腺癌(LUAC)是常见的肺肿瘤之一,死亡率高。recq样解旋酶4 (RECQL4)基因已被发现作为癌基因参与不同癌症的进展,并与LUAC预后不良有关。森皮质(CM)提取物已被研究影响细胞进程调节不同的疾病。然而,RECQL4和CM提取物的详细功能以及它们在LUAC中的调节机制尚未阐明。本研究旨在探讨RECQL4和CM提取物对LUAC进展的影响。RECQL4在LUAC中的表达通过The Cancer Genome Atlas (TCGA)数据库进行评估。实时定量聚合酶链反应检测RECQL4 mRNA表达。Western blot检测细胞间质转化过程(epithelial-mesenchymal transition [EMT] process)、核因子κB (NF-κB)和细胞外信号调节激酶(ERK)信号通路相关蛋白的表达。通过细胞计数试剂盒-8检测细胞增殖情况。创面愈合和transwell实验证实了细胞的迁移和侵袭。通过衰老相关β -半乳糖苷酶染色评估细胞衰老情况。流式细胞术检测细胞周期。我们的研究结果表明,RECQL4在LUAC组织和细胞系中表现出更高的表达。通过功能实验,我们发现RECQL4促进细胞增殖、迁移和侵袭以及EMT进展。此外,RECQL4还能缓解细胞周期阻滞和细胞衰老。此外,RECQL4通过提高LUAC中phospho(p) -p65-p65和p-ERK -ERK水平激活NF-κB和ERK信号通路。CM提取物在LUAC中具有抗肿瘤作用,可阻断recql4诱导的NF-κB和ERK信号通路。我们的研究结果表明,CM提取物通过阻断recql4诱导的NF-κB和ERK信号通路来抑制LUAC细胞的迁移和侵袭。这一结果为LUAC的治疗提供了一个有希望的治疗策略。
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