Department of Internal Medicine, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Department of Respiratory and Critical Medicine, The Second Affiliated Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Oncol Rep. 2019 Apr;41(4):2518-2528. doi: 10.3892/or.2019.6994. Epub 2019 Feb 1.
Chromatin assembly factor 1 subunit B (CHAF1B) participates in DNA synthesis and repair. High CHAF1B expression has been associated with a poor prognosis in several types of cancers. However, no study has evaluated the clinical significance and biological function of CHAF1B in non‑small cell lung cancer (NSCLC). In the present study, we aimed to investigate CHAF1B expression and its role in NSCLC. In the present study, it was revealed that CHAF1B was highly expressed in NSCLC lung tissues and 95‑D cells. Kaplan‑Meier survival analysis indicated that high CHAF1B expression in tumour tissue was associated with poor clinical outcomes in NSCLC patients. Multivariate Cox analyses revealed that lymph node metastasis, tumour‑node‑metastasis (TNM) stage and CHAF1B expression were independent prognostic factors in NSCLC patients. Moreover, CHAF1B knockdown in 95‑D cells markedly inhibited tumour proliferation, reduced colony formation, induced cell cycle arrest and promoted apoptosis. In vivo studies demonstrated that CHAF1B knockdown inhibited the growth of transplanted tumours. Furthermore, our results revealed that the mechanism by which CHAF1B induced apoptosis was mediated by the activation of the p53‑dependent apoptotic signalling pathway (BAK/Bcl‑2/caspase‑3) in 95‑D cells. These data indicated that CHAF1B plays an important role in tumourigenesis and may be a therapeutic molecular target to counter NSCLC progression.
染色质组装因子 1 亚基 B（CHAF1B）参与 DNA 合成和修复。CHAF1B 高表达与多种类型癌症的不良预后相关。然而，尚无研究评估 CHAF1B 在非小细胞肺癌（NSCLC）中的临床意义和生物学功能。在本研究中，我们旨在研究 CHAF1B 在 NSCLC 中的表达及其作用。本研究表明，CHAF1B 在 NSCLC 肺组织和 95-D 细胞中高表达。Kaplan-Meier 生存分析表明，肿瘤组织中 CHAF1B 高表达与 NSCLC 患者的临床结局不良相关。多变量 Cox 分析显示，淋巴结转移、肿瘤-淋巴结-转移（TNM）分期和 CHAF1B 表达是 NSCLC 患者的独立预后因素。此外，在 95-D 细胞中敲低 CHAF1B 显著抑制肿瘤增殖，减少集落形成，诱导细胞周期停滞并促进细胞凋亡。体内研究表明，敲低 CHAF1B 抑制了移植瘤的生长。此外，我们的结果表明，CHAF1B 通过激活 p53 依赖性凋亡信号通路（BAK/Bcl-2/caspase-3）诱导凋亡的机制在 95-D 细胞中发挥作用。这些数据表明，CHAF1B 在肿瘤发生中发挥重要作用，可能是对抗 NSCLC 进展的治疗分子靶标。
