LINC01089 functions as a ceRNA for miR-152-3p to inhibit non‐small lung cancer progression through regulating PTEN

Cancer Cell International

Huixian Zhang¹  Xingya Li¹  Di Geng¹  Siyuan Huang¹  Qianqian Guo¹  Hao Zhang² 

[1] Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo.1 Jianshe East Road, 450052, Zhengzhou, Henan, China;Department of Radiology, Changhai Hospital Affiliated to The Second Military Medical University, No.168 Changhai Road, 200433, Shanghai, China;

关键词: LINC01089;    NSCLC;    miR-152-3p;    PTEN;   

DOI  :  10.1186/s12935-021-01846-7

来源: Springer

【 摘 要 】

BackgroundLong 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.MethodsThe 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.ResultsLINC01089 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.ConclusionsDown-regulation of LINC01089 promoted the progression of NSCLC through regulating miR-152-3p/PTEN axis.

【 授权许可】

CC BY