Evidence map›Paper›PMID 33318617›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2021

LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia.

Zhen-Jiang Li, Jing Cheng, Yuan Song, Hui-Hui Li, Ji-Fu Zheng

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  4. The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025
    Review
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  19. The Vital Roles of LINC00662 in Human Cancers.Frontiers in cell and developmental biology · 2021
    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

5 authors at 1 institution in 1 country.

Zhen-Jiang LiDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China.
Jing ChengDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China.
Yuan SongDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China.
Hui-Hui LiDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China.
Ji-Fu ZhengDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China. ncjeff@163.com.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and the underlying mechanisms. The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.

Indexed as

AdultCell Line, TumorCell SurvivalConnective Tissue Growth FactorFemaleHumansLeukemia, Myeloid, AcuteMaleMicroRNAsNeovascularization, PathologicRNA, Long NoncodingSignal TransductionUp-RegulationVascular Endothelial Growth Factor AYY1 Transcription FactorCCN2 protein, humanConnective Tissue Growth Factorlong non-coding RNA SNHG5, humanMicroRNAsMIRN26 microRNA, humanRNA, Long NoncodingVascular Endothelial Growth Factor AVEGFA protein, humanYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID33318617
OpenAlexW3111589013

What OpenQuestion holds

Textmetadata
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.