Evidence map›Paper›PMID 33913391›Full record

ArticleScience progress

MiR-326 mediates malignant biological behaviors of lung adenocarcinoma by targeting ZEB1.

Mingxin Liu, Hong Wu, Yiqiang Liu, Yan Tan, Songtao Wang, Shaohua Xie, Run Xiang, Jingchen Liang, Ru Zhang, Chuan Xu and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science progress. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Mingxin LiuSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.ORCID 0000-0002-4800-1219
Hong WuSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Yiqiang LiuIntegrative Cancer Center & Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan, Cancer Center, School of Medicine University, Sichuan, China.
Yan TanThe General Hospital of Western Theater Command, Chengdu, Sichuan, China.
Songtao WangThe General Hospital of Western Theater Command, Chengdu, Sichuan, China.
Shaohua XieSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Run XiangSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Jingchen LiangIntegrative Cancer Center & Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan, Cancer Center, School of Medicine University, Sichuan, China.
Ru ZhangThe General Hospital of Western Theater Command, Chengdu, Sichuan, China.
Chuan XuSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Jintao HeSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Qiang LiSchool of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
University of Electronic Science and Technology of China · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiR-326 functions as an antioncogene in the several types of cancer. However, the underling mechanisms through which miRNA-326 regulates the anti-carcinogenesis of lung adenocarcinoma have remained elusive. The aim of this study was to explore the role and regulatory mechanism of miR-326 in cell proliferation, invasion, migration and apoptosis in lung adenocarcinoma. Quantitative real-time PCR (qRT-PCR) was used to detect the expression pattern of miR-326 in human bronchial epithelial cells (HBES-2B), 4 kinds of lung adenocarcinoma cell lines (H23, H1975, H2228, H2085) and 20 lung adenocarcinoma tissues. Then, H23 cells were infected with miR-326 mimics, miR-326 inhibitors and si-ZEB1 to build up-regulated miR-326 cell lines, down-regulated ZEB1(zinc-finger-enhancer binding protein 1)cell lines, simultaneous down-regulated ZEB1 and miR-326 cell lines. Moreover, CCK-8 assay, transwell invasion assay, wound healing assay and flow cytometry assay were employed to examine the effects of miR-326 and ZEB1 on the proliferation, invasion, migration and apoptosis abilities of H23 cells. Western blot was performed to explore the effects of miR-326 and ZEB1 on the expression of invasion and migration related proteins N-cadherin, E-cadherin, MMP7, MMP13, SLUG and apoptotic proteins PARP, BAX. On the mechanism, a dual-luciferase reporter gene was used to measure the target relationship between miR-326 and ZEB1. MiR-326 expression was significantly downregulated in lung adenocarcinoma tissues and cells. Overexpression of miR-326 significantly inhibited the malignant behaviors of H23 cells. Mechanically, luciferase reporter assay showed that ZEB1 was a direct target of miR-326. MiR-326 mimic downregulated the expression of ZEB1. Furthermore, knocking down ZEB1 strongly inhibited the proliferation, invasion and migration of H23 cells but promoted apoptosis. MiR-326 could target ZEB1 to inhibit the proliferation, invasion and migration of lung adenocarcinoma cells and promote apoptosis, which is a potential therapeutic target for lung adenocarcinoma.

Indexed as

AdenocarcinomaAdenocarcinoma of LungLung NeoplasmsMicroRNAsZinc Finger E-box-Binding Homeobox 1Cell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansMicroRNAsMIRN326 microRNA, humanZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1epithelial mesenchymal transitionLung adenocarcinomamalignant biological behaviorsmiR-326zinc-finger-enhancer binding protein 1

Identifiers

PMID33913391
PMCPMC10454963
OpenAlexW3159221696

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.