Evidence map›Paper›PMID 30796205›Full record

ArticleCell death & disease2019

MiR-15b and miR-322 inhibit SETD3 expression to repress muscle cell differentiation.

Meng-Jie Zhao, Jun Xie, Wen-Jie Shu, Hong-Yan Wang, Jianping Bi, Wei Jiang, Hai-Ning Du

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Bone and muscle crosstalk in ageing and disease.Nature reviews. Endocrinology · 2025
    Review
  4. Article
  5. Molecular communication from bone to skeletal muscle: an overview.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. miR-424(322)-5p targetsActa biochimica et biophysica Sinica · 2023
    Article
  10. Article
  11. Genistein Promotes Skeletal Muscle Regeneration by Regulating miR-221/222.International journal of molecular sciences · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

Meng-Jie ZhaoHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, 430072, Wuhan, China.
Jun XieHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, 430072, Wuhan, China.
Wen-Jie ShuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, 430072, Wuhan, China.
Hong-Yan WangHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, 430072, Wuhan, China.
Jianping BiHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, 430072, Wuhan, China.
Wei JiangMedical Research Institute, School of Medicine, Wuhan University, 430071, Wuhan, China.
Hai-Ning DuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, 430072, Wuhan, China. hainingdu@whu.edu.cn.ORCID http://orcid.org/0000-0001-8062-5411
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SETD3 is a member of SET-domain containing methyltransferase family, which plays critical roles in various biological events. It has been shown that SETD3 could regulate the transcription of myogenic regulatory genes in C2C12 differentiation and promote myoblast determination. However, how SETD3 is regulated during myoblast differentiation is still unknown. Here, we report that two important microRNAs (miRNAs) could repress SETD3 and negatively contribute to myoblast differentiation. Using microRNA (miRNA) prediction engines, we identify and characterize miR-15b and miR-322 as the primary miRNAs that repress the expression of SETD3 through directly targeting the 3'-untranslated region of SETD3 gene. Functionally, overexpression of miR-15b or miR-322 leads to the repression of endogenous SETD3 expression and the inhibition of myoblast differentiation, whereas inhibition of miR-15b or miR-322 derepresses endogenous SETD3 expression and facilitates myoblast differentiation. In addition, knockdown SETD3 in miR-15b or miR-322 repressed myoblasts is able to rescue the facilitated differentiation phenotype. More interestingly, we revealed that transcription factor E2F1 or FAM3B positively or negatively regulates miR-15b or miR-322 expression, respectively, during muscle cell differentiation, which in turn affects SETD3 expression. Therefore, our results establish two parallel cascade regulatory pathways, in which transcription factors regulate microRNAs fates, thereby controlling SETD3 expression and eventually determining skeletal muscle differentiation.

Indexed as

3' Untranslated RegionsAnimalsCell DifferentiationCytokinesE2F1 Transcription FactorHEK293 CellsHistone MethyltransferasesHumansMiceMicroRNAsMuscle DevelopmentMyoblastsNeoplasm Proteins3' Untranslated RegionsCytokinesE2F1 protein, humanE2F1 Transcription FactorFAM3B protein, humanHistone MethyltransferasesMicroRNAsMIRN15 microRNA, humanMIRN424 microrna, humanNeoplasm ProteinsSetd3 protein, mouse

Identifiers

PMID30796205
PMCPMC6385263
OpenAlexW2915103810

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.