Evidence map›Paper›PMID 30106218›Full record

ArticleThoracic cancer2018

MiR-520b restrains cell growth by targeting HDAC4 in lung cancer.

Ke Jin, Weixin Zhao, Xuan Xie, Yuejiang Pan, Kexi Wang, Huizhong Zhang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  6. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
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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

6 authors at 2 institutions in 1 country.

Ke JinDepartment of Thoracic Surgery, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Weixin ZhaoDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xuan XieDepartment of Thoracic Surgery, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Yuejiang PanDepartment of Thoracic Surgery, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Kexi WangDepartment of Thoracic Surgery, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Huizhong ZhangDepartment of Thoracic Surgery, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.ORCID 0000-0001-5903-1643
Sun Yat-sen University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs) function as tumor promoting or tumor suppressing factors in many cancers. MiR-520b contributes to progression in head-neck and liver cancers, spinal osteosarcoma, and glioma; however, the association of miR-520b with lung cancer progression remains unknown. In this investigation, we explore the effect of miR-520b targeting HDAC4 on lung cancer growth.

methodsThe regulation of miR-520b or its inhibitor on HDAC4 expression was analyzed using Western blot analysis. After treatment of miR-520b or its inhibitor, miR-520b and HDAC4 levels were examined using quantitative real time-PCR. The modulation of miR-520b on HDAC4 was investigated by luciferase reporter gene assay. Cell proliferation evaluation was performed using colony formation and methyl-thiazolyl-tetrazolium assays. The correlation between miR-520b and HDAC4 in human clinical samples was verified using Pearson's correlation coefficient.

resultsAn obvious decrease in HDAC4 expression was observed in lung cancer A549 cells treated with different doses of miR-520b. The miR-520b inhibitor enhanced HDAC4 expression in lung cancer cells. Bioinformatics predicted the targeting of miR-520b on HDAC4. MiR-520b directly targeted the 3' untranslated region of HDAC4. The introduction of miR-520b obviously inhibited cell proliferation in vitro. Anti-miR-520b was capable of accelerating lung cancer cell proliferation; however, HDAC4 knockdown destroyed anti-miR-520b-induced cell proliferation. Finally, a negative correlation between miR-520b and HDAC4 was observed in clinical human lung cancer samples.

conclusionMiR-520b decreases HDAC4 expression to control cell proliferation in lung cancer.

Indexed as

3' Untranslated RegionsA549 CellsCell Line, TumorCell ProliferationDisease ProgressionDown-RegulationHistone DeacetylasesHumansLung NeoplasmsMicroRNAsRepressor ProteinsTransfection3' Untranslated RegionsHDAC4 protein, humanHistone DeacetylasesMicroRNAsMIRN520 microRNA, humanRepressor ProteinsGrowthHDAC4lung cancermiR-520b

Identifiers

PMID30106218
PMCPMC6166052
OpenAlexW2886270794

What OpenQuestion holds

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LicenceCC BY-NC
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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.