Department of Thoracic Surgery, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
Mol Carcinog. 2019 Nov;58(11):1933-1945. doi: 10.1002/mc.23072. Epub 2019 Sep 5.
Lung cancer is one of the most common causes of cancer-related mortality worldwide, which is partially due to its metastasis. However, the mechanism underlying its metastasis remains elusive. In this study, we showed that a low Krüppel-like factor 3 (KLF3) expression level is correlated with a poor prognosis and TNM stages in clinical patients with lung cancer and further demonstrated that KLF3 expression is downregulated in lung cancer tissues compared with adjacent normal samples. In addition, bioinformatics analysis results showed that KLF3 expression is related to lung cancer epithelial-mesenchymal transition (EMT). In vitro and in vivo experiments also showed that KLF3 silencing promotes lung cancer EMT and enhances lung cancer metastasis. More importantly, bioinformatics analysis and in vitro experiments indicated that the role of KLF3 in lung cancer metastasis is dependent on the STAT3 signaling pathway. Overall, our data indicated the crucial function of KLF3 in lung cancer metastasis and suggested opportunities to improve the therapy of patients with lung cancer.
肺癌是全球癌症相关死亡的最常见原因之一，部分原因是其转移。然而，其转移的机制仍不清楚。在这项研究中，我们表明低 Krüppel 样因子 3（KLF3）表达水平与肺癌临床患者的预后不良和 TNM 分期相关，并进一步表明与相邻正常样本相比，肺癌组织中 KLF3 表达下调。此外，生物信息学分析结果表明，KLF3 表达与肺癌上皮-间充质转化（EMT）有关。体外和体内实验也表明，KLF3 沉默促进肺癌 EMT 并增强肺癌转移。更重要的是，生物信息学分析和体外实验表明，KLF3 在肺癌转移中的作用依赖于 STAT3 信号通路。总的来说，我们的数据表明 KLF3 在肺癌转移中具有重要作用，并为改善肺癌患者的治疗提供了机会。
