Zhang Haihua, Li Junqiang, Tian Feng, Su Xuan, Wang Xinxin, Tang Di, Zhang Lei, Zhang Tao, Ni Yunfeng
Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Department of Oncology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Front Oncol. 2022 May 5;12:897553. doi: 10.3389/fonc.2022.897553. eCollection 2022.
The RNA-binding protein quaking homolog 6 (QKI-6) is a tumor-suppressor gene in several cancers. However, its role in non-small cell lung cancer (NSCLC) is unclear. In this study, we aimed to determine the association between QKI-6 expression and survival and clinicopathological features in patients with NSCLC and identify the related mechanisms. Western blot and immunohistochemistry (IHC) were used to detect QKI-6 expression in NSCLC. The effect of QKI-6 on NSCLC cells was determined by overexpression and knockdown assays, and label-free quantitative proteomics and Western blot were used to identify the underlying mechanisms. Low QKI-6 expression level was positively correlated with poor overall survival in patients with NSCLC. Furthermore, QKI-6 overexpression inhibited NSCLC cell proliferation and migration and induced a block in the G0/G1 phase, and QKI-6 downregulation increased proliferation and migration. QKI-6 inhibited EMT processes EGFR/SRC/STAT3 signaling by upregulating AGR2. In conclusion, QKI-6 could be used to develop novel strategies for the treatment of NSCLC.
RNA结合蛋白震颤同源物6(QKI-6)在多种癌症中是一种肿瘤抑制基因。然而,其在非小细胞肺癌(NSCLC)中的作用尚不清楚。在本研究中,我们旨在确定QKI-6表达与NSCLC患者生存及临床病理特征之间的关联,并确定相关机制。采用蛋白质免疫印迹法和免疫组织化学(IHC)检测NSCLC中QKI-6的表达。通过过表达和敲低实验确定QKI-6对NSCLC细胞的影响,并采用无标记定量蛋白质组学和蛋白质免疫印迹法确定潜在机制。NSCLC患者中低QKI-6表达水平与较差的总生存期呈正相关。此外,QKI-6过表达抑制NSCLC细胞增殖和迁移,并诱导细胞阻滞于G0/G1期,而QKI-6下调则增加细胞增殖和迁移。QKI-6通过上调AGR2抑制EMT过程中的EGFR/SRC/STAT3信号传导。总之,QKI-6可用于开发治疗NSCLC的新策略。