LINC01089, deleted by YY1, inhibits lung cancer progression by targeting the miR-301b-3p / HPDG axis

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Cell Biol Toxicol. September 24, 2021. doi: 10.1007 / s10565-021-09643-8. Online ahead of print.

ABSTRACT

OBJECTIVE: LINC01089 is a newly identified and rarely reported lncRNA in human cancers. Our study aimed to investigate its role in lung cancer.

METHODS: YY1, LINC01089, and levels of miR-301b-3p in lung cancer tissues and cells were assessed using qRT-PCR. Bioinformatics analyzes and luciferase reporter assays, ChIP and RIP were performed to determine the relationships between YY1, LINC01089, miR-301b-3p and HPGD. Gain and loss of function tests were performed to confirm the impacts of LINC01089 and HPDG in lung cancer cells. The CCK-8 assay was used to assess the rate of cell proliferation, and the Transwell assay was applied to measure cell invasion and migration. An in vivo tumor model was applied to validate the role of LINC01089.

RESULTS: LINC01089 decreased in lung cancer tissues and cells, and low level of LINC01089 predicted poor clinical outcome. YY1 directly bound to the LINC01089 promoter region and inhibited its transcription. LINC01089 knockdown thwarted the proliferation, invasion and migration capacity of H1299 and A549 cells and worsened tumor growth. Specifically, LINC01089 functioned as an endogenous RNA competing with miR-301b-3p to modulate HPGD and thus affected lung cancer progression.

CONCLUSION: Our data revealed that LINC01089, directly suppressed by YY1, inhibited lung cancer progression by targeting the miR-301b-3p / HPGD axis. Graphic Summary 1. Expression of LINC01089 was downregulated in lung cancer tissues and cell lines, and low levels of LINC01089 predicted poor clinical outcome. 2. LINC01089 knockdown enhanced proliferation, invasion and migration of H1299 and A549 cells in vitro and promoted tumorigenesis and metastasis of lung cancer cells in vivo. 3. LINC01089, directly deleted by YY1, functioned as an endogenous RNA competitor against miR-301b-3p to increase expression of HPGD.

IDPM: 34561789 | DOI: 10.1007 / s10565-021-09643-8


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Shawn Beecher

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