LncRNA MIR100HG Affects the Proliferation and Metastasis of Lung Cancer Cells Through Mediating the MicroRNA-5590-3p/DCBLD2 Axis

Overview

Journal Immun Inflamm Dis

Specialties Allergy & Immunology
Infectious Diseases

Date 2024 Apr 11

PMID 38602284

Authors

Shengping Min

Linxiang Zhang

Li Zhang

Fangfang Liu

Miao Liu

Affiliations

Soon will be listed here.

Abstract

Objective: The aim of this paper is to investigate the effect of long noncoding RNA (lncRNA) MIR100HG on the proliferation and metastasis of lung cancer cells by mediating the microRNA (miR)-5590-3p/DCBLD2 axis.

Methods: RNA levels of MIR100HG, miR-5590-3p, and DCBLD2 in lung cancer tissues and cells were detected by quantitative reverse-transcription polymerase chain reaction, and protein level was assessed by Western blot. Effects of MIR100HG or miR-5590-3p on proliferation, migration, and invasion of lung cancer cells were detected by Cell Counting Kit-8, colony formation, and Transwell assays. Luciferase reporter assay and RNA-immunoprecipitation assay confirmed the target relationship between miR-5590-3p and MIR100HG or DCBLD2.

Results: MIR100HG and DCBLD2 were highly expressed, while miR-5590-3p was lowly expressed in lung cancer tissues and cells. Silencing MIR100HG or upregulating miR-5590-3p impeded lung cancer cell proliferation, migration, and invasion. MIR100HG could up-regulate DCBLD2 by sponging miR-5590-3p. Downregulation of miR-5590-3p partly overturned the suppressive effect of silencing MIR100HG on lung cancer cell proliferation and metastasis, and overexpression of DCBLD2 also reversed the effect of overexpression of miR-5590-3p on lung cancer cell proliferation and metastasis.

Conclusion: LncRNA MIR100HG promotes lung cancer progression by targeting and negatively regulating DCBLD2 through binding with miR-5590-3p.

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LncRNA MIR100HG affects the proliferation and metastasis of lung cancer cells through mediating the microRNA-5590-3p/DCBLD2 axis.

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