Evidence map›Paper›PMID 34769245›Full record

ArticleInternational journal of molecular sciences2021

LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte.

Liping Zhang, Junyi Hu, Bahar I Meshkat, Kenneth W Liechty, Junwang Xu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 51 citations in OpenAlex.

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  20. The Journey of Cancer Cells to the Brain: Challenges and Opportunities.International journal of molecular sciences · 2023
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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

5 authors at 2 institutions in 1 country.

Liping ZhangDepartment of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Junyi HuLaboratory for Fetal and Regenerative Biology, Department of Surgery, University of Colorado Denver-Anschutz Medical Campus and Children's Hospital Colorado, Aurora, CO 80045, USA.ORCID 0000-0003-4461-2482
Bahar I MeshkatDepartment of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Kenneth W LiechtyLaboratory for Fetal and Regenerative Biology, Department of Surgery, University of Colorado Denver-Anschutz Medical Campus and Children's Hospital Colorado, Aurora, CO 80045, USA.
Junwang XuDepartment of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
University of Tennessee Health Science Center · USChildren's Hospital Colorado · US

Funding

The role of long non-coding RNA GAS5 in diabetic woundsR01GM128660 · NIGMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI XU, JUNWANG · 2019 to 2023
$1.5M
NIGMS NIH HHS R01 GM128660NIH HHS GM128660
6 · The paper itself

Abstract

One of the major complications in diabetes is impaired wound healing. Unfortunately, effective therapies are currently lacking. Epithelial to mesenchymal transition (EMT) is a critical process involved in cutaneous wound healing. In response to injury, EMT is required to activate and mobilize stationary keratinocytes in the skin toward the wound bed, which allows for re-epithelialization. This process is stalled in diabetic wounds. In this study, we investigate the role of long non-coding RNA (lncRNA), MALAT1, in transforming growth factor beta 1(TGF-β1)-induced EMT of human keratinocyte (HaCaT) cells. Initially, we detected MALAT1 and TGF-β1 expression in non-diabetic and diabetic wounds and found that these expression are significantly up-regulated in diabetic wounds. Then, HaCaT cells were cultured and exposed to TGF-β1. The EMT of HaCaT cells were confirmed by the increased expression of CDH2, KRT10, and ACTA2, in addition to the down-regulation of CDH1. Knockdown of MALAT1 was achieved by transfecting a small interfering RNA (SiRNA). MALAT1 silencing attenuates TGFβ1-induced EMT. Mechanistically, MALAT1 is involved in TGF-β1 mediated EMT through significantly induced ZEB1 expression, a critical transcription factor for EMT. In summary, lncRNA MALAT1 is involved in TGFβ1-induced EMT of human HaCaT cells and provides new understanding for the pathogenesis of diabetic wounds.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsCell LineFemaleHumansKeratinocytesMiceRNA, Long NoncodingTransforming Growth Factor beta1MALAT1 long non-coding RNA, humanMalat1 long non-coding RNA, mouseRNA, Long NoncodingTGFB1 protein, humanTgfb1 protein, mouseTransforming Growth Factor beta1diabetic woundsepithelial mesenchymal transitionlong non-coding RNAMALAT1

Identifiers

PMID34769245
PMCPMC8584148
OpenAlexW3208952168

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.