Cui Yuxin, Li Zhilei, Cao Junxia, Lane Jane, Birkin Emily, Dong Xuefei, Zhang Lijian, Jiang Wen G
Cardiff China Medical Research Collaborative, School of Medicine, Cardiff University, Cardiff, United Kingdom.
Department of Pharmacy, Zhujiang Hospital of Southern Medical University, Guangzhou, China.
Front Oncol. 2021 Apr 27;11:655757. doi: 10.3389/fonc.2021.655757. eCollection 2021.
Lung cancer is one of the most prevalent cancers in both men and women worldwide. The nucleic acid G4 structures have been implicated in the transcriptional programmes of cancer-related genes in some cancers such as lung cancer. However, the role of the dominant G4 resolvase DHX36 in the progression of lung cancer remains unknown. In this study, by bioinformatic analysis of public datasets (TCGA and GEO), we find DHX36 is an independent prognosis indicator in non-small-cell lung carcinoma (NSCLC) with subtype dependence. The stable lentiviral knockdown of the DHX36 results in accelerated migration and aggregation of the S-phase subpopulation in lung cancer cells. The reduction of DHX36 level de-sensitises the proliferation response of lung cancer cells to chemotherapeutic drugs such as paclitaxel with cell dependence. The knockdown of this helicase leads to promoted tumour growth, demonstrated by a 3D fluorescence spheroid lung cancer model, and the stimulation of cell colony formation as shown by single-cell cultivation. High throughput proteomic array indicates that DHX36 functions in lung cancer cells through regulating multiple signalling pathways including activation of protein activity, protein autophosphorylation, Fc-receptor signalling pathway, response to peptide hormone and stress-activated protein kinase signalling cascade. A causal transcriptomic analysis suggests that DHX36 is significantly associated with mRNA surveillance, RNA degradation, DNA replication and Myc targets. Therefore, we unveil that DHX36 presents clinical significance and plays a role in tumour suppression in lung cancer, and propose a potentially new concept for an anti-cancer therapy based on helicase-specific targeting.
肺癌是全球男性和女性中最常见的癌症之一。核酸G4结构已在某些癌症(如肺癌)中涉及癌症相关基因的转录程序。然而,主要的G4解旋酶DHX36在肺癌进展中的作用仍然未知。在本研究中,通过对公共数据集(TCGA和GEO)进行生物信息学分析,我们发现DHX36是具有亚型依赖性的非小细胞肺癌(NSCLC)中的一个独立预后指标。稳定的慢病毒介导的DHX36敲低导致肺癌细胞中S期亚群的迁移和聚集加速。DHX36水平的降低使肺癌细胞对化疗药物(如紫杉醇)的增殖反应失去敏感性,且具有细胞依赖性。通过3D荧光球体肺癌模型证明,这种解旋酶的敲低导致肿瘤生长促进,单细胞培养显示细胞集落形成受到刺激。高通量蛋白质组学阵列表明,DHX36通过调节多种信号通路在肺癌细胞中发挥作用,包括蛋白质活性激活、蛋白质自磷酸化、Fc受体信号通路、对肽激素的反应和应激激活蛋白激酶信号级联反应。因果转录组分析表明,DHX36与mRNA监测、RNA降解、DNA复制和Myc靶点显著相关。因此,我们揭示了DHX36在肺癌中具有临床意义并发挥肿瘤抑制作用,并提出了基于解旋酶特异性靶向的潜在抗癌治疗新概念。