Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Department of Pulmonary and Critical Care Medicine, Huadu District People's Hospital of Guangzhou, Guangzhou, China.
Comput Math Methods Med. 2022 Jan 30;2022:3193553. doi: 10.1155/2022/3193553. eCollection 2022.
Research in this article was performed to explore the biological role and clinical significance of Krüppel-like transcription factor 6 (KLF6) in non-small-cell lung cancer (NSCLC).
KLF6 expression in NSCLC cell lines was analyzed using reverse transcription PCR and Western blot. The expressed KLF6 protein was examined in 50 surgical NSCLC tissues using immunohistochemistry. Statistical analyses were employed for clinical association examinations. CCK8 assay and Annexin V/PI analysis were used to execute cell proliferation and apoptosis in KLF6-overexpression cell lines and the control groups. Cleaved caspase-3 expression was also detected in KLF6-overexpression cells and NSCLC tissues. KLF6 expression correlation with cleaved caspase-3 was also examined.
It was discovered that downregulation of KLF6 was seen in human NSCLC cell lines. Low KLF6 expression in NSCLC tissues was correlated with poor patient prognosis ( < 0.005); patients with less KLF6 expression possessed a lower cumulative 5-year survival rate. Multivariate analysis showed KLF6 expression as an independent prognostic indicator for NSCLC individuals. Expression levels of KLF6 were associated with NSCLC tumor size ( = 0.041). Overexpression of KLF6 inhibited cell proliferation and stimulated A549 and H322 cell line apoptosis. Cleaved caspase-3 protein had higher expression levels in KLF6-overexpressed cells than in the control group. The KLF6 expression levels were positively related to the cleaved caspase-3 protein expression in NSCLC tissues ( = 0.689, = 0.001).
The results indicate that downregulation of KLF6 is a significant NSCLC progression marker. KLF6 prevents cell growth and promotes cell apoptosis, possibly caspase-3 activations.
本研究旨在探讨 Krüppel 样转录因子 6(KLF6)在非小细胞肺癌(NSCLC)中的生物学作用和临床意义。
采用逆转录 PCR 和 Western blot 分析 NSCLC 细胞系中 KLF6 的表达。采用免疫组织化学法检测 50 例手术 NSCLC 组织中表达的 KLF6 蛋白。采用统计学分析进行临床关联检验。CCK8 检测和 Annexin V/PI 分析用于执行 KLF6 过表达细胞系和对照组的细胞增殖和凋亡。还检测了 KLF6 过表达细胞和 NSCLC 组织中 cleaved caspase-3 的表达。还检查了 KLF6 表达与 cleaved caspase-3 的相关性。
发现 KLF6 在人 NSCLC 细胞系中下调。NSCLC 组织中 KLF6 低表达与患者预后不良相关(<0.005);KLF6 表达较少的患者累积 5 年生存率较低。多变量分析显示 KLF6 表达是非小细胞肺癌患者的独立预后指标。KLF6 的表达水平与 NSCLC 肿瘤大小相关(=0.041)。过表达 KLF6 抑制细胞增殖并刺激 A549 和 H322 细胞系凋亡。Cleaved caspase-3 蛋白在 KLF6 过表达细胞中的表达水平高于对照组。KLF6 表达水平与 NSCLC 组织中 cleaved caspase-3 蛋白表达呈正相关(=0.689,=0.001)。
结果表明,KLF6 的下调是非小细胞肺癌进展的重要标志物。KLF6 可防止细胞生长并促进细胞凋亡,可能通过激活 caspase-3。