Zhou Lili, Xing Chen, Zhou Dongxia, Yang Rong, Cai Maohuai
Department of Oncology, Yancheng Second People's Hospital, No. 135 Kaifang Avenue, Yancheng 224003, Jiangsu, China.
Open Med (Wars). 2020 Oct 8;15(1):986-996. doi: 10.1515/med-2020-0219. eCollection 2020.
Non-small-cell lung carcinoma (NSCLC) seriously threatens the health of human beings. Aberrant expression of lncRNAs has been confirmed to be related with the progression of multiple malignant tumors, including NSCLC. LncRNA FGF12-AS2 has been considered to be upregulated in NSCLC. However, the mechanism by which FGF12-AS2 promotes the tumorigenesis of NSCLC remains elusive.
Gene and protein expressions in NSCLC cells were measured by q-PCR and western blot, respectively. CCK-8 and immunofluorescence staining were performed to detect the cell proliferation. Cell apoptosis was tested by flow cytometry. Transwell assay was used to detect the cell migration and invasion. Finally, the dual luciferase report assay was used to verify the relation among FGF12-AS2, miR-188-3p, and NCAPG2.
Downregulation of FGF12-AS2 significantly inhibited the proliferation of NSCLC cells via inducing apoptosis. In addition, FGF12-AS2 silencing notably suppressed the migration and invasion of A549 cells. Meanwhile, FGF12-AS2 modulated the progression of NSCLC via regulation of miR-188-3p/NCAPG2 axis. Finally, knockdown of FGF12-AS2 inhibited the tumorigenesis of NSCLC via suppressing the EMT process of NSCLC.
Downregulation of lncRNA FGF12-AS2 suppressed the tumorigenesis of NSCLC via sponging miR-188-3p. Thus, FGF12-AS2 may serve as a potential target for the treatment of NSCLC.
非小细胞肺癌(NSCLC)严重威胁人类健康。长链非编码RNA(lncRNAs)的异常表达已被证实与包括NSCLC在内的多种恶性肿瘤的进展有关。lncRNA FGF12-AS2在NSCLC中被认为是上调的。然而,FGF12-AS2促进NSCLC肿瘤发生的机制仍不清楚。
分别采用q-PCR和蛋白质免疫印迹法检测NSCLC细胞中的基因和蛋白质表达。进行CCK-8和免疫荧光染色以检测细胞增殖。通过流式细胞术检测细胞凋亡。采用Transwell实验检测细胞迁移和侵袭。最后,使用双荧光素酶报告实验验证FGF12-AS2、miR-188-3p和NCAPG2之间的关系。
FGF12-AS2的下调通过诱导凋亡显著抑制NSCLC细胞的增殖。此外,FGF12-AS2沉默显著抑制A549细胞的迁移和侵袭。同时,FGF12-AS2通过调节miR-188-3p/NCAPG2轴调节NSCLC的进展。最后,FGF12-AS2的敲低通过抑制NSCLC的上皮-间质转化(EMT)过程抑制NSCLC的肿瘤发生。
lncRNA FGF12-AS2的下调通过海绵吸附miR-188-3p抑制NSCLC的肿瘤发生。因此,FGF12-AS2可能作为NSCLC治疗的潜在靶点。