Evidence map›Paper›PMID 36473369›Full record

ArticleClinics (Sao Paulo, Brazil)2023

LIM-domain binding protein 2 was down-regulated by miRNA-96-5p inhibited the proliferation, invasion and metastasis of lung cancer H1299 cells.

Fuying Chu, Xinxin Xu, Yan Zhang, Hua Cai, Jingjing Peng, Yanan Li, Han Zhang, Hongli Liu, Xiang Chen

Open access · goldAbstract read
In one paragraph

Article in Clinics (Sao Paulo, Brazil), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 7 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

9 authors at 2 institutions in 1 country.

Fuying ChuDepartment of Laboratory Medicine, Nantong First People's Hospital, China.
Xinxin XuDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, China.
Yan ZhangDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, China.
Hua CaiDepartment of Laboratory Medicine, Affiliated Hospital of Nantong University, China.
Jingjing PengDepartment of Laboratory Medicine, Nantong First People's Hospital, China.
Yanan LiDepartment of Laboratory Medicine, Nantong First People's Hospital, China.
Han ZhangDepartment of Laboratory Medicine, Nantong First People's Hospital, China.
Hongli LiuDepartment of Laboratory Medicine, Nantong Tumor Hospital, China.
Xiang ChenDepartment of Laboratory Medicine, Nantong First People's Hospital, China. Electronic address: ntchenx0521@163.com.
Nantong University · CNNantong Tumor Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesLung cancer was one of the most common malignancies around the world. It has great significance in to search for the mechanism of occurrence and development of lung cancer. LIM Domain Binding protein 2 (LDB2) belongs to the LIM-domain binding family, it can be used as a binding protein that combined with other transcription factors to form the transcription complex for regulating the expression of target genes. The expression of microRNA-96-5p (miR-96-5p) has been investigated in various tumors. The aim of this study is to investigate the potential role of LDB2 and miR-96-5p in lung cancer.

methodsReal-time quantitative PCR was applied to detect the expression of LDB2 and miR-96-5p. The proliferation, invasion, and metastasis of H1299 cells were analyzed by CCK8, transwell, and wound healing assay after LDB2 or miR-96-5p transfection. Luciferase activities assay and western blot were used to reveal the targeted regulation between LDB2 and miR-96-5p.

resultsHere the authors found LDB2 was down-regulated in lung cancer tissues and negatively correlated with miR-96-5p expression, it could promote or inhibit the proliferation, invasion and metastasis of H1299 cells after LDB2 knockdown or overexpression and regulate the expression of cyclinD1, MMP9, Bcl-2, and Bax via ERK1/2 signaling pathway. Furthermore, miR-96-5p exerted its function by directly binding to 3'-UTR of LDB2 and regulating expression of LDB2. miR-96-5p could promote the proliferation, invasion, and metastasis of H1299 cells.

conclusionThese findings demonstrate that LDB2 can act as a new regulator to inhibit cell proliferation, invasion, and metastasis via the ERK1/2 signaling pathway, and miR-96-5p may be a potential promising molecular by targeting LDB2 in lung cancer.

Indexed as

Lung NeoplasmsMicroRNAs3' Untranslated RegionsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansLIM Domain ProteinsNeoplasm InvasivenessTranscription Factors3' Untranslated RegionsLDB2 protein, humanLIM Domain ProteinsMicroRNAsMIRN96 microRNA, humanTranscription FactorsInvasionLDB2Lung cancerMetastasismiR-96-5pProliferation

Identifiers

PMID36473369
PMCPMC9727592
OpenAlexW4311430695

What OpenQuestion holds

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LicenceCC BY
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.