Evidence map›Paper›PMID 35181869›Full record

ArticleMolecular biotechnology2022

MiR-139-5p Targeting CCNB1 Modulates Proliferation, Migration, Invasion and Cell Cycle in Lung Adenocarcinoma.

Bin Bao, Xiaojun Yu, Wujun Zheng

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Regulatory Role ofInternational journal of molecular sciences · 2024
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  19. [Screening and validation of pivotal genes in hepatitis B virus-associated hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
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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

3 authors at 2 institutions in 1 country.

Bin BaoCardiothoracic Surgery Department, The First People's Hospital of Fuyang, No. 429, Beihuan Road, Fuchun Street, Fuyang District, Hangzhou, 311400, Zhejiang, China. BBaoin0214@163.com.ORCID http://orcid.org/0000-0001-9312-5096
Xiaojun YuCardiothoracic Surgery Department, The First People's Hospital of Fuyang, No. 429, Beihuan Road, Fuchun Street, Fuyang District, Hangzhou, 311400, Zhejiang, China.
Wujun ZhengCardiothoracic Surgery Department, The First People's Hospital of Fuyang, No. 429, Beihuan Road, Fuchun Street, Fuyang District, Hangzhou, 311400, Zhejiang, China.
The First People's Hospital of Guiyang · CNFuyang City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is the most frequent histological subtype of non-small cell lung cancer. Cyclin B1 (CCNB1) is the vital initiator and controller of mitosis. Studies have indicated that CCNB1 overexpression is closely associated with cell proliferation and tumorigenesis in many cancers. Thus, discovery of molecular mechanism of CCNB1 in LUAD is conducive to developing new diagnostic or therapeutic targets for LUAD. We acquired mature miRNA and mRNA expression information of LUAD from TCGA database, as well as related clinical data. CCNB1 expression in normal and LUAD tissue was analyzed. Relationship between CCNB1 and patient's survival and clinical stage was analyzed. Upstream regulatory gene miRNA of CCNB1 was predicted. qRT-PCR and western blot examined expression levels of CCNB1 and miR-139-5p in cells. CCK-8 tested cell proliferation. Scratch healing and Transwell determined cell migration and invasion. Flow cytometry analyzed the cell cycle. Dual-luciferase verified targeting relationship between the two genes. Compared to controls, CCNB1 expression was prominently high in LUAD patient samples, and associated with advanced tumor stages and shorter overall survival. MiR-139-5p expressed an evidently negative correlation with CCNB1 and was predicted to target CCNB1. MiR-139-5p mimics reduced CCNB1 mRNA and protein expression, and suppressed luciferase activity in a target-specific manner, as confirmed by a control construct with a mutated miR-139-5p binding site. CCNB1 overexpression fostered progression of LUAD cells. Mechanistically, miR-139-5p might negatively regulate CCNB1 in LUAD, thereby suppressing cell proliferation, migration, invasion and cell cycle.

Indexed as

Adenocarcinoma of LungCarcinoma, Non-Small-Cell LungCyclin B1Lung NeoplasmsMicroRNAsCell CycleCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansRNA, MessengerCCNB1 protein, humanCyclin B1MicroRNAsMIRN139 microRNA, humanRNA, MessengerCCNB1InvasionLung adenocarcinomaMigrationmiR-139-5pProliferation

Identifiers

PMID35181869
OpenAlexW4213247093

What OpenQuestion holds

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Registered trials

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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.