Evidence map›Paper›PMID 33926524›Full record

ArticleClinical epigenetics2021

HDAC2 enhances esophageal squamous cell carcinoma development through down-regulating microRNA-503-5p and promoting CXCL10.

Jindong Li, Chengyan Jin, Lihua Sun, Bin Wang, Peiyan Hua, Yan Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. 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

6 authors at 1 institution in 1 country.

Jindong LiDepartment of Thoracic Surgery, The Second Hospital of Jilin University, NO. 218 Ziqiang Street, Changchun, 130041, Jilin, China.
Chengyan JinDepartment of Thoracic Surgery, The Second Hospital of Jilin University, NO. 218 Ziqiang Street, Changchun, 130041, Jilin, China.
Lihua SunDepartment of Anesthesiology, The Second Hospital of Jilin University, Changchun, 130041, Jilin, China.
Bin WangDepartment of Thoracic Surgery, The Second Hospital of Jilin University, NO. 218 Ziqiang Street, Changchun, 130041, Jilin, China.
Peiyan HuaDepartment of Thoracic Surgery, The Second Hospital of Jilin University, NO. 218 Ziqiang Street, Changchun, 130041, Jilin, China.
Yan ZhangDepartment of Thoracic Surgery, The Second Hospital of Jilin University, NO. 218 Ziqiang Street, Changchun, 130041, Jilin, China. Zhangyan943@outlook.com.ORCID 0000-0002-9382-533X
Second Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAlthough esophageal squamous cell carcinoma (ESCC)-oriented mechanism has been widely explored, the integrated action of histone deacetylase 2 (HDAC2), microRNA (miR)-503-5p and C-X-C motif chemokine 10 (CXCL10) in ESCC has not been thoroughly explored. Thus, we performed the research to study the role of HDAC2/miR-503-5p/CXCL10 axis in ESCC.

methodsESCC tissues and mucosal tissues (5 cm from cancer tissues) were collected, in which HDAC2, miR-503-5p and CXCL10 expression levels were tested. The mechanism of HDAC2, miR-503-5p and CXCL10 was interpreted. The viability, colony formation ability, apoptosis, invasion and migration abilities of ESCC cells were tested after HDAC2, miR-503-5p or CXCL10 expression was altered. Tumorigenesis in mice was observed to further verify the in vitro effects of HDAC2 and miR-503-5p.

resultsHDAC2 and CXCL10 were up-regulated while miR-503-5p was down-regulated in ESCC. HDAC2 bound to miR-503-5p and miR-503-5p targeted CXCL10. Silencing HDAC2 or restoring miR-503-5p depressed viability, colony-forming, invasion and migration abilities and enhanced apoptosis of ESCC cells in vitro, as well as suppressed ESCC tumorigenesis in vivo. Inhibition of miR-503-5p or elevation of CXCL10 negated HDAC2 knockout-induced effects on ESCC cells.

conclusionThis work elucidates that HDAC2 knockdown retards the process of ESCC by elevating miR-503-5p and inhibiting CXCL10 expression, which may provide a guidance for ESCC management.

Indexed as

AdultAgedAnimalsChemokine CXCL10Disease Models, AnimalDown-RegulationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticHistone Deacetylase 2HumansMaleMiceMice, NudeMicroRNAsChemokine CXCL10CXCL10 protein, humanHDAC2 protein, humanHistone Deacetylase 2MicroRNAsMIRN503 microRNA, humanApoptosisC-X-C motif chemokine 10Esophageal squamous cell carcinomaHistone deacetylase 2MicroRNA-503-5pTumorigenesis

Identifiers

PMID33926524
PMCPMC8082674
OpenAlexW3159891700

What OpenQuestion holds

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LicenceCC BY
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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.