Evidence map›Paper›PMID 37017854›Full record

ArticleIrish journal of medical science2023

CCT6A promotes esophageal squamous cell carcinoma cell proliferation, invasion and epithelial-mesenchymal transition by activating TGF-β/Smad/c-Myc pathway.

Xiuli Xia, Shushan Zhao, Wenting Chen, Chao Xu, Dongqiang Zhao

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Article in Irish journal of medical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Chaperonin in health and disease.Molecular biomedicine · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
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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 3 institutions in 1 country.

Xiuli XiaDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China.
Shushan ZhaoDepartment of Gastroenterology, Handan Central Hospital, Handan, 056001, China.
Wenting ChenDepartment of Endoscopy Center, The First Affiliated Hospital of Hebei North University, Zhangjiakou, 075000, China.
Chao XuDepartment of Gastroenterology, Handan Central Hospital, Handan, 056001, China.
Dongqiang ZhaoDepartment of Gastroenterology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, China. hbzdq1998@163.com.ORCID http://orcid.org/0000-0002-4458-4816
Handan College · CNHebei Medical University · CNHebei North University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChaperonin-containing TCP1 subunit 6A (CCT6A) facilitates several malignant cancer behaviors, but its regulation of esophageal squamous cell carcinoma (ESCC) has not been reported. This study aimed to investigate the effect of CCT6A on cell proliferation, apoptosis, invasion and epithelial-mesenchymal transition (EMT) and its interaction with the TGF-β/Smad/c-Myc pathway in ESCC.

methodsCCT6A expression was detected in ESCC and normal esophageal epithelial cell lines by RT‒qPCR and western blotting. Furthermore, CCT6A siRNA, negative control (NC) siRNA, CCT6A encoding plasmid and NC encoding plasmid were transfected into OE21 and TE-1 cells. Subsequently, CCT6A siRNA- and NC siRNA-transfected cells were treated with TGF-β for rescue experiments. Cell proliferation, apoptosis, invasion, and E-cadherin/N-cadherin and p-Smad2/p-Smad3/c-Myc expression were detected.

resultsCCT6A expression was increased in KYSE-180, TE-1, TE-4 and OE21 cells compared with HET-1A cells. In both OE21 and TE-1 cells, CCT6A knockdown inhibited cell proliferation, invasion and N-cadherin expression while promoting cell apoptosis and E-cadherin expression; meanwhile, CCT6A overexpression had the opposite effects. Furthermore, in both OE21 and TE-1 cells, CCT6A knockdown decreased p-Smad2/Smad2, p-Smad3/Smad3 and c-Myc/GAPDH expression; CCT6A overexpression had the opposite effects. Next, TGF-β facilitated cell proliferation, invasion, and N-cadherin, p-Smad2/Smad2, p-Smad3/Smad2 and c-Myc/GAPDH expression while repressing cell apoptosis and E-cadherin expression in OE21 and TE-1 cells; importantly, TGF-β could compensate for the regulation of CCT6A knockdown on these activities.

conclusionCCT6A facilitates ESCC malignant activities by activating the TGF-β/Smad/c-Myc pathway, which sheds light on the identification of a possible therapeutic target in the management of ESCC.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaCadherinsCell Line, TumorCell MovementCell ProliferationChaperonin Containing TCP-1Epithelial-Mesenchymal TransitionHumansRNA, Small InterferingTransforming Growth Factor betaCadherinsCCT6A protein, humanChaperonin Containing TCP-1RNA, Small InterferingTransforming Growth Factor betaCCT6AEpithelial-mesenchymal transitionEsophageal squamous cell carcinomaTGF-β/Smad/c-Myc pathwayViability and mobility

Identifiers

PMID37017854
OpenAlexW4362602669

What OpenQuestion holds

Textmetadata
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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.