Huixian Zhang1, Hao Zhang2, Xingya Li3, Siyuan Huang3, Qianqian Guo3, Di Geng3. 1. Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo.1 Jianshe East Road, Zhengzhou, 450052, Henan, China. huixianzhang0406@163.com. 2. Department of Radiology, Changhai Hospital Affiliated to The Second Military Medical University, No.168 Changhai Road, Shanghai, 200433, China. 3. Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Νo.1 Jianshe East Road, Zhengzhou, 450052, Henan, China.
Abstract
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.
BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to exert crucial functions in regulating the progression of humancancers. 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.
Authors: Fan Yang; Xiaoli Fan; Yifeng Liu; Yi Shen; Shenglan Zhao; Yanyi Zheng; Ruoting Men; Yan Xie; Li Yang Journal: Front Pharmacol Date: 2021-12-06 Impact factor: 5.810