马拉特1
细胞凋亡
癌症研究
长非编码RNA
细胞生长
核糖核酸
肺癌
小RNA
细胞
编码(社会科学)
生物
细胞生物学
医学
肿瘤科
遗传学
基因
统计
数学
作者
J. J. Song,Su Zz,Q. Shen
出处
期刊:DOAJ: Directory of Open Access Journals - DOAJ
日期:2020-02-01
被引量:13
摘要
Objective Non-small cell lung cancer (NSCLC) is a common type of lung cancer. Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was reported to play a tumor-promoting role in NSCLC; however, the regulatory mechanism of MALAT1 in NSCLC progression remains largely unknown. Materials and methods The expression levels of MALAT1, miR-374b-5p and SRSF7 were measured by quantitative real-time polymerase chain reaction (qRT-PCR), and the protein level of SRSF7 was detected by Western blot analysis. Cell proliferation and apoptosis were determined by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Cell migration and invasion were assessed by transwell assay. In addition, starBase3.0 software and dual-luciferase reporter assay were used to identify the correlations between miR-374b-5p and MALAT1 or SRSF7. Nude mouse xenograft assay was performed to explore the effects of MALAT1 on NSCLC in vivo. Results We first observed that the levels of MALAT1 and SRSF7 were upregulated while miR-374b-5p was downregulated in NSCLC tissues; meanwhile, the expression level of MALAT1 was negatively correlated with miR-374b-5p and positively correlated with SRSF7. Both knockdown of MALAT1 and miR-374b-5p overexpression inhibited proliferation, migration and invasion and induced apoptosis in NSCLC cells. Then, we identified that miR-374b-5p was a target of MALAT1 and SRSF7 was the downstream of miR-374b-5p. In addition, overexpression of SRSF7 reversed the effects of MALAT1 knockdown on proliferation, apoptosis, migration and invasion in NSCLC cells. Finally, overexpression of MALAT1 suppressed NSCLC tumor growth in vivo. Conclusions Our results demonstrated that MALAT1 contributed to NSCLC progression through the MALAT1/miR-374b-5p/SRSF7 axis.
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