Evidence map›Paper›PMID 31878829›Full record

ArticleCell cycle (Georgetown, Tex.)2020

Long non-coding RNA HOXA11-AS accelerates the progression of keloid formation via miR-124-3p/TGFβR1 axis.

Jun Jin, Zhen-Hua Jia, Xiao-Hua Luo, Hong-Feng Zhai

RetractedOpen access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.3field-weighted citation impact, top 4% 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, 41 citations in OpenAlex.

  1. Review
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  7. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jun JinDepartment of Plastic Surgery, People's Hospital of Zhengzhou University, Henan People's Hospital, Zhengzhou, P.R. China.
Zhen-Hua JiaDepartment of Plastic Surgery, People's Hospital of Zhengzhou University, Henan People's Hospital, Zhengzhou, P.R. China.
Xiao-Hua LuoDepartment of Plastic Surgery, People's Hospital of Zhengzhou University, Henan People's Hospital, Zhengzhou, P.R. China.
Hong-Feng ZhaiDepartment of Plastic Surgery, People's Hospital of Zhengzhou University, Henan People's Hospital, Zhengzhou, P.R. China.ORCID 0000-0002-8960-9888
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence reveals the importance of long non-coding RNAs (lncRNAs) in the development and progression of keloid formation, whereas the underlying mechanisms are not well understood. In the present study, we investigated the biological effects and molecular mechanisms of lncRNA HOXA11-AS in keloid formation. First, the expression levels of HOXA11-AS, miR-124-3p, and transforming growth factor β receptor type I (TGFβR1) were measured in both keloid tissues and human keloid fibroblasts (HKFs) using qRT-PCR and western blot analysis, respectively. Next, we adopted both gain- and loss-of-function strategies to explore the significance of HOXA11-AS. TUNEL, flow cytometry, DNA ladder, and tube formation assays were performed to measure cell apoptosis and angiogenesis, respectively. Besides, the potential binding relationship between HOXA11-AS and miR-124-3p, as well as miR-124-3p and TGFβR1 was identified using bioinformatic screening and verified by luciferase reporter assay. Furthermore, we explored the importance of miR-124-3p in HOXA11-AS-induced phenotypes and regulations on TGFβ signaling or PI3K/Akt signaling. We found that HOXA11-AS and TGFβR1 were significantly up-regulated, while miR-124-3p was down-regulated both in keloid tissues or fibroblasts than in normal skin tissues or fibroblasts. Functionally, high expression of HOXA11-AS essentially inhibited cell apoptosis and promoted fibroblast-induced angiogenesis. Mechanistically, miR-124-3p was identified as a downstream effector to be involved in HOXA11-AS-mediated phenotypes through directly targeting TGFβR1, thus modulating PI3K/Akt signaling pathway. Taken together, our findings revealed that HOXA11-AS inhibits cell apoptosis and promotes angiogenesis through miR-124-3p/TGFβR1 axis, contributing to the progression of keloid formation, which might provide a novel target for keloid therapy.

Indexed as

Disease ProgressionSignal TransductionAdultApoptosisBase SequenceDown-RegulationFemaleFibroblastsHumansKeloidMaleMicroRNAsMiddle AgedNeovascularization, PhysiologicPhenotypePhosphatidylinositol 3-KinasesMicroRNAsMIRN124 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Transforming Growth Factor-beta Type IRNA, Long NoncodingTGFBR1 protein, humanKeloid formationlncRNA HOXA11-ASmiR-124-3pTGFβ receptor type I

Identifiers

PMID31878829
PMCPMC6961662
OpenAlexW2996860690

What OpenQuestion holds

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Registered trials

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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.