Literature DB >> 31010333

Long noncoding RNA LINC-PINT inhibits non-small cell lung cancer progression through sponging miR-218-5p/PDCD4.

Libin Zhang1, Jing Hu2, Jiagui Li1, Qiuju Yang3, Menghui Hao4, Liang Bu1,5.   

Abstract

Long noncoding RNA, long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was showed to be involved in cancer development. However, the biological effect of LINC-PINT on non-small cell lung cancer (NSCLC) remains unknown. Here, we aimed to investigate the role and underlying mechanism of LINC-PINT in NSCLC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the level of LINC-PINT in NSCLC tissues and cell lines. Cell counting kit-8 (CCK-8), flow cytometry, migration and transwell invasion assays were used to investigate cell proliferation, cell cycle, cell migration and invasion, respectively. The targets of LINC-PINT were verified by both luciferase reporter assay and RNA immunoprecipitation assay. Tumour xenografts were used to reveal the effect of LINC-PINT on tumourigenesis in vivo. We observed that LINC-PINT expression increased in both NSCLC tissues and cell lines. Function assays exhibited that LINC-PINT reduced NSCLC cell proliferation, cell cycle, cell migration and invasion in vitro. We also indicated that LINC-PINT mediated inhibitory effect on cell proliferation, cell cycle, cell migration and invasion by miR-208a-3p/programmed cell death 4 (PDCD4) in NSCLC cells. These findings indicated that LINC-PINT functions as a tumour-suppressor that exerts important regulatory roles in NSCLC progression by sponging miR-208a-3p/PDCD4.

Entities:  

Keywords:  LINC-PINT; Non-small cell lung cancer; PDCD4; miR-208a-3p

Mesh:

Substances:

Year:  2019        PMID: 31010333     DOI: 10.1080/21691401.2019.1605371

Source DB:  PubMed          Journal:  Artif Cells Nanomed Biotechnol        ISSN: 2169-1401            Impact factor:   5.678


  14 in total

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10.  Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4.

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