Evidence map›Paper›PMID 31754329›Full record

ArticleInternational journal of biological sciences2019

EGF suppresses the expression of miR-124a in pancreatic β cell lines via ETS2 activation through the MEK and PI3K signaling pathways.

Lin Yang, Yuansen Zhu, Delin Kong, Jiawei Gong, Wen Yu, Yang Liang, Yuzhe Nie, Chun-Bo Teng

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  13. MicroRNA-mediated regulation of glucose and lipid metabolism.Nature reviews. Molecular cell biology · 2021
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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

8 authors at 1 institution in 1 country.

Lin YangCollege of Life Science, Northeast Forestry University, Harbin, China.
Yuansen ZhuCollege of Life Science, Northeast Forestry University, Harbin, China.
Delin KongCollege of Life Science, Northeast Forestry University, Harbin, China.
Jiawei GongCollege of Life Science, Northeast Forestry University, Harbin, China.
Wen YuCollege of Life Science, Northeast Forestry University, Harbin, China.
Yang LiangCollege of Life Science, Northeast Forestry University, Harbin, China.
Yuzhe NieCollege of Life Science, Northeast Forestry University, Harbin, China.
Chun-Bo TengCollege of Life Science, Northeast Forestry University, Harbin, China.
Northeast Forestry University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is characterized by pancreatic β cell dysfunction. Previous studies have indicated that epidermal growth factor (EGF) and microRNA-124a (miR-124a) play opposite roles in insulin biosynthesis and secretion by beta cells. However, the underlying mechanisms remain poorly understood. In the present study, we demonstrated that EGF could inhibit miR-124a expression in beta cell lines through downstream signaling pathways, including mitogen-activated protein kinase kinase (MEK) and phosphatidylinositol 3-kinase (PI3K) cascades. Further, the transcription factor ETS2, a member of the ETS (E26 transformation-specific) family, was identified to be responsible for the EGF-mediated suppression of miR-124a expression, which was dependent on ETS2 phosphorylation at threonine 72. Activation of ETS2 decreased miR-124a promoter transcriptional activity through the putative conserved binding sites AGGAANA/TN in three miR-124a promoters located in different chromosomes. Of note, ETS2 played a positive role in regulating beta cell function-related genes, including miR-124a targets, Forkhead box a2 (FOXA2) and Neurogenic differentiation 1 (NEUROD1), which may have partly been through the inhibition of miR-124 expression. Knockdown and overexpression of ETS2 led to the prevention and promotion of insulin biosynthesis respectively, while barely affecting the secretion ability. These results suggest that EGF may induce the activation of ETS2 to inhibit miR-124a expression to maintain proper beta cell functions and that ETS2, as a novel regulator of insulin production, is a potential therapeutic target for diabetes mellitus treatment.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBinding SitesDiabetes MellitusEpidermal Growth FactorFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHepatocyte Nuclear Factor 3-betaInsulinInsulin-Secreting CellsIslets of LangerhansMiceMice, Inbred C57BLMicroRNAsMitogen-Activated Protein KinasesBasic Helix-Loop-Helix ProteinsEpidermal Growth FactorETS2 protein, humanFoxa2 protein, mouseHepatocyte Nuclear Factor 3-betaInsulinMicroRNAsMirn124 microRNA, mouseMitogen-Activated Protein KinasesNeurod1 protein, mousePhosphatidylinositol 3-KinaseProto-Oncogene Protein c-ets-2ThreonineBeta cellsEGFR signalingETS2Insulin.MicroRNA-124a

Identifiers

PMID31754329
PMCPMC6854373
OpenAlexW2976994154

What OpenQuestion holds

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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.