LINC01089作为miR-152-3p的竞争性内源RNA，通过调控PTEN来抑制非小细胞肺癌的进展。
LINC01089 functions as a ceRNA for miR-152-3p to inhibit non-small lung cancer progression through regulating PTEN.
作者信息
Zhang Huixian, Zhang Hao, Li Xingya, Huang Siyuan, Guo Qianqian, Geng Di
机构信息
Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo.1 Jianshe East Road, Zhengzhou, 450052, Henan, China.
Department of Radiology, Changhai Hospital Affiliated to The Second Military Medical University, No.168 Changhai Road, Shanghai, 200433, China.
出版信息
Cancer Cell Int. 2021 Mar 2;21(1):143. doi: 10.1186/s12935-021-01846-7.
BACKGROUND
Long non-coding RNAs (lncRNAs) have been reported to exert crucial functions in regulating the progression of human cancers. However, the function and mechanism of long intergenic non-protein coding RNA 01089 (LINC01089) in non-small cell lung cancer (NSCLC) have not been revealed.
METHODS
The expression level of LINC01089, microRNA (miRNA, miR)-152-3p and phosphatase and tensin homolog deleted onc hromosome ten (PTEN) mRNA was detected by quantitative real-time PCR (qRT-PCR). After gain-of-function and loss-of-function models were established with NSCLC cell lines, the proliferation, migration and invasion of NSCLC cells were detected by cell counting kit-8 (CCK-8) assay, scratch healing assay, Transwell assay, respectively. Dual luciferase reporter assay was employed to validate the binding relationship between miR-152-3p and LINC01089 or the 3'UTR of PTEN. Western blot was used to detect PTEN expression in NSCLC cells after LINC01089 and miR-152-3p were selectively modulated.
RESULTS
LINC01089 was down-regulated in NSCLC tissues and cells. Functional experiments showed that knockdown of LINC01089 could promote the proliferation, migration and invasion of NSCLC cells, while over-expression of LINC01089 had the opposite effects. miR-152-3p was identified as a functional target for LIN01089, and miR-152-3p could reverse the function of LINC01089. Additionally, LINC01089 could up-regulate the expression level of PTEN via repressing miR-152-3p.
CONCLUSIONS
Down-regulation of LINC01089 promoted the progression of NSCLC through regulating miR-152-3p/PTEN axis.
背景
据报道，长链非编码RNA（lncRNAs）在调节人类癌症进展中发挥关键作用。然而，长链基因间非编码RNA 01089（LINC01089）在非小细胞肺癌（NSCLC）中的功能和机制尚未明确。
方法
采用定量实时聚合酶链反应（qRT-PCR）检测LINC01089、微小RNA（miRNA，miR）-152-3p和第10号染色体缺失的磷酸酶及张力蛋白同源物（PTEN）mRNA的表达水平。在用NSCLC细胞系建立功能获得和功能缺失模型后，分别通过细胞计数试剂盒-8（CCK-8）检测、划痕愈合检测、Transwell检测来检测NSCLC细胞的增殖、迁移和侵袭能力。采用双荧光素酶报告基因检测法验证miR-152-3p与LINC01089或PTEN的3'非翻译区（3'UTR）之间的结合关系。在选择性调节LINC01089和miR-152-3p后，用蛋白质免疫印迹法检测NSCLC细胞中PTEN的表达。
结果
LINC01089在NSCLC组织和细胞中表达下调。功能实验表明，敲低LINC01089可促进NSCLC细胞的增殖、迁移和侵袭，而LINC01089过表达则产生相反的效果。miR-152-3p被确定为LINC01089的功能靶点，miR-152-3p可逆转LINC01089的功能。此外，LINC01089可通过抑制miR-152-3p上调PTEN的表达水平。
结论
LINC01089的下调通过调节miR-152-3p/PTEN轴促进了NSCLC的进展。
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