Evidence map›Paper›PMID 31872383›Full record

ArticleGenes & genomics2020

miR-489 suppresses multiple myeloma cells growth through inhibition of LDHA-mediated aerobic glycolysis.

Han Wu, Xiuhong Wang, Tingting Wu, Su Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Genes & genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  5. Review
  6. MicroRNAs as Regulators of Cancer Cell Energy Metabolism.Journal of personalized medicine · 2022
    Review
  7. Review
  8. Review
  9. UCHL3 promotes aerobic glycolysis of pancreatic cancer through upregulating LDHA expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  10. Article
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  12. Article
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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

4 authors at 2 institutions in 1 country.

Han WuDepartment of Clinical Laboratory Medicine, Sir Run Run Shaw Hospital Xiasha Campus, Zhejiang University School of Medicine, 368 Xiasha Road, Jianggan District, Hangzhou, 310018, Zhejiang, China. 3684203wuhan@zju.edu.cn.
Xiuhong WangDepartment of Clinical Laboratory Medicine, Sir Run Run Shaw Hospital Xiasha Campus, Zhejiang University School of Medicine, 368 Xiasha Road, Jianggan District, Hangzhou, 310018, Zhejiang, China.
Tingting WuDepartment of Clinical Laboratory Medicine, Sir Run Run Shaw Hospital Xiasha Campus, Zhejiang University School of Medicine, 368 Xiasha Road, Jianggan District, Hangzhou, 310018, Zhejiang, China.
Su YangDepartment of Clinical Laboratory Medicine, Sir Run Run Shaw Hospital Xiasha Campus, Zhejiang University School of Medicine, 368 Xiasha Road, Jianggan District, Hangzhou, 310018, Zhejiang, China.
Sir Run Run Shaw Hospital · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDysregulation of miR-489 in human tumors has been widely reported. Lactate dehydrogenase isoform A (LDHA)-mediated aerobic glycolysis participates in proliferation of multiple myeloma (MM) cells.

objectiveTo investigate whether miR-489 induced MM growth inhibition via targeting to LDHA-mediated aerobic glycolysis.

methodsExpression of miR-489 in representative MM cell lines was determined via qRT-PCR (quantitative real-time polymerase chain reaction). MTT (3-(4, 5-di methyl thiazol-2-yl)-2, 5-di phenyl tetrazolium bromide) and colony formation assays were utilized to detect cell viability and proliferation. Effect of miR-489 on aerobic glycolysis was detected via glucose uptake, lactate and ATP production. Binding ability between miR-489 and LDHA was conducted via luciferase activity assay.

resultsMiR-489 was down-regulated in representative MM cell lines. Gain-of functional assays indicated that over-expression of miR-489 decreased cell viability and inhibited cell proliferation of MM cells. Moreover, miR-489 inhibited aerobic glycolysis via decrease of glucose uptake, lactate and ATP production. LDHA was identified as target of miR-489, suggesting a negative correlation between miR-489 and LDHA in MM cells. Mechanically, the inhibition ability of miR-489 on proliferation of MM cells was through inhibition of LDHA-mediated aerobic glycolysis.

conclusionsmiR-489 inhibited MM tumor growth via LDHA-mediated glycolytic metabolism, suggesting potential therapeutic target ability of miR-489/LDHA for MM.

Indexed as

Cell Line, TumorCell ProliferationCell SurvivalDown-RegulationGene Expression Regulation, NeoplasticGlycolysisHumansLactate Dehydrogenase 5MicroRNAsMultiple MyelomaLactate Dehydrogenase 5MicroRNAsMIRN489 microRNA, humanAerobic glycolysisLDHAmiR-489Multiple myelomaProliferation

Identifiers

PMID31872383
OpenAlexW2996073933

What OpenQuestion holds

Textmetadata
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.