Evidence map›Paper›PMID 36672841›Full record

ArticleGenes2022

MYC Causes Multiple Myeloma Progression via Attenuating TP53-Induced MicroRNA-34 Expression.

Yuki Murakami, Kei Kimura-Masuda, Tsukasa Oda, Ikuko Matsumura, Yuta Masuda, Rei Ishihara, Saki Watanabe, Yuko Kuroda, Tetsuhiro Kasamatsu, Nanami Gotoh and 5 more

Open access · goldAbstract read
In one paragraph

Article in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.3field-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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Heliyon · 2023
    Review
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

15 authors at 2 institutions in 1 country.

Yuki MurakamiDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Kei Kimura-MasudaDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Tsukasa OdaLaboratory of Mucosal Ecosystem Design, The Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8510, Japan.ORCID 0000-0002-8941-161X
Ikuko MatsumuraDepartment of Hematology, Gunma University Graduate School of Medicine, Maebashi 371-8510, Japan.
Yuta MasudaDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.ORCID 0000-0002-6923-6199
Rei IshiharaDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Saki WatanabeDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Yuko KurodaDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Tetsuhiro KasamatsuDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Nanami GotohDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Hisashi TakeiDepartment of Hematology, Gunma University Graduate School of Medicine, Maebashi 371-8510, Japan.
Nobuhiko KobayashiDepartment of Hematology, Gunma University Graduate School of Medicine, Maebashi 371-8510, Japan.ORCID 0000-0002-3341-5566
Takayuki SaitohDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi 371-8510, Japan.
Hirokazu MurakamiFaculty of Medical Technology and Clinical Engineering, Gunma University of Health and Welfare, Maebashi 371-0823, Japan.
Hiroshi HandaDepartment of Hematology, Gunma University Graduate School of Medicine, Maebashi 371-8510, Japan.ORCID 0000-0003-3753-9862
Gunma University · JPGunma University of Health and Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs and miRs) are small (19-25 base pairs) non-coding RNAs with the ability to modulate gene expression. Previously, we showed that the miR-34 family is downregulated in multiple myeloma (MM) as the cancer progressed. In this study, we aimed to clarify the mechanism of miRNA dysregulation in MM. We focused particularly on the interaction between MYC and the TP53-miR34 axis because there is a discrepancy between increased TP53 and decreased miR-34 expressions in MM. Using the nutlin-3 or Tet-on systems, we caused wild-type (WT) p53 protein accumulation in human MM cell lines (HMCLs) and observed upregulated miR-34 expression. Next, we found that treatment with an Myc inhibitor alone did not affect miR-34 expression levels, but when it was coupled with p53 accumulation, miR-34 expression increased. In contrast, forced MYC activation by the MYC-ER system reduced nutlin-3-induced miR-34 expression. We also observed that TP53 and MYC were negatively correlated with mature miR-34 expressions in the plasma cells of patients with MM. Our results suggest that MYC participates in the suppression of p53-dependent miRNA expressions. Because miRNA expression suppresses tumors, its inhibition leads to MM development and malignant transformation.

Indexed as

MicroRNAsMultiple MyelomaCell Line, TumorCell Transformation, NeoplasticHumansTumor Suppressor Protein p53MicroRNAsMIRN34 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53epigeneticsmicroRNAmultiple myelomaMYCp53

Identifiers

PMID36672841
PMCPMC9859619
OpenAlexW4313362221

What OpenQuestion holds

Textmetadata
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.