Evidence map›Paper›PMID 38061883›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2023

[Mechanism of miR-186-5p Regulating PRKAA2 to Promote Ferroptosis 
in Lung Adenocarcinoma Cells].

Lu Liu, Xin Guan, Yanqiao Zhao, Xiaona Wang, Chonggao Yin, Qinghua Liu, Hongli Li

Open access · greenAbstract readEnglish Abstract
PubMed Full text at PMC Publisher
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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2 citing papers in PubMed, 2 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Lu LiuDepartment of Pathhology, Weifang Medical University, Weifang 261053, China.
Xin GuanClinical Medical College, Weifang Medical University, Weifang 261053, China.
Yanqiao ZhaoDepartment of Pathhology, Weifang Medical University, Weifang 261053, China.
Xiaona WangDepartment of Pathhology, Weifang Medical University, Weifang 261053, China.
Chonggao YinColloge of Nursing, Weifang Medical University, Weifang 261053, China.
Qinghua LiuCollege of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China.
Hongli LiMedical Research Center, Weifang Medical University, Weifang 261053, China.
Weifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2.

methodsPrevious investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bioinformatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PRKAA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PRKAA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PRKAA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD cells were measured using the L-ROS tests to determine the effects of miR-186-5p and PRKAA2.

resultsThe expression of PRKAA2 is up-regulated, and a high level of PRKAA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRKAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRKAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRKAA2.

conclusionsmiR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRKAA2, thus inhibiting the proliferation, invasion and migration of LUAD.
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Indexed as

3,4-MethylenedioxyamphetamineAdenocarcinoma of LungCarcinoma, Non-Small-Cell LungFerroptosisLung NeoplasmsMicroRNAsAMP-Activated Protein KinasesCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansHyperaldosteronismReactive Oxygen Species3,4-MethylenedioxyamphetamineAMP-Activated Protein KinasesMicroRNAsMIRN186 microRNA, humanPRKAA2 protein, humanReactive Oxygen SpeciesFerroptosisInvasionLung neoplasmsMigrationmiR-186-5pPRKAA2Proliferation

Identifiers

PMID38061883
PMCPMC10714044
OpenAlexW4389803415

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.