Yin Li, Wang Ji-peng, Xu Tong-peng, Chen Wen-ming, Huang Ming-de, Xia Rui, Liu Xin-xin, Kong Rong, Sun Ming, Zhang Er-bao, Shu Yong-qian
Department of Oncology, the First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, People's Republic of China.
Tumour Biol. 2015 Apr;36(4):3075-84. doi: 10.1007/s13277-014-2943-4. Epub 2014 Dec 14.
Kruppel-like factor 2 (KLF2) expression is diminished in many malignancies. However, its expression and role in nonsmall-cell lung cancer (NSCLC) remain unknown. In this study, we found that KLF2 levels were decreased in NSCLC tissues compared with adjacent normal tissues. Its expression level was significantly correlated with TNM stages, tumor size, and lymph node metastasis. Moreover, patients with low levels of KLF2 expression had a relatively poor prognosis. Furthermore, knockdown of KLF2 expression by siRNA could promote cell proliferation, while ectopic expression of KLF2 inhibited cell proliferation and promoted apoptosis in NSCLC cells partly via regulating CDKN1A/p21 and CDKN2B/p15 protein expression. Our findings present that decreased KLF2 could be identified as a poor prognostic biomarker in NSCLC and regulate cell proliferation and apoptosis.
Kruppel样因子2（KLF2）在许多恶性肿瘤中表达降低。然而，其在非小细胞肺癌（NSCLC）中的表达及作用仍不清楚。在本研究中，我们发现与相邻正常组织相比，NSCLC组织中KLF2水平降低。其表达水平与TNM分期、肿瘤大小及淋巴结转移显著相关。此外，KLF2表达水平低的患者预后相对较差。此外，通过小干扰RNA（siRNA）敲低KLF2表达可促进细胞增殖，而KLF2的异位表达部分通过调节细胞周期蛋白依赖性激酶抑制剂1A（CDKN1A）/p21和细胞周期蛋白依赖性激酶抑制剂2B（CDKN2B）/p15蛋白表达抑制NSCLC细胞增殖并促进细胞凋亡。我们的研究结果表明，KLF2降低可被鉴定为NSCLC中预后不良的生物标志物，并调节细胞增殖和凋亡。
