Evidence map›Paper›PMID 36453704›Full record

ArticleMolecular carcinogenesis2023

Circ-E-Cad encodes a protein that promotes the proliferation and migration of gastric cancer via the TGF-β/Smad/C-E-Cad/PI3K/AKT pathway.

Fanying Li, Hongxing Tang, Shaoji Zhao, Xinya Gao, Lixuan Yang, Jianbo Xu

Open access · hybridAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Coding circular RNA in human cancer.Genes & diseases · 2025
    Review
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  10. Circular RNA-Encoded Proteins in Disease Pathogenesis.International journal of biological sciences · 2025
    Review
  11. Article
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  13. Article
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  17. Circular RNAs Variously Participate in Coronary Atherogenesis.Current issues in molecular biology · 2023
    Review
  18. Review
  19. 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

6 authors at 2 institutions in 1 country.

Fanying LiDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Hongxing TangDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Shaoji ZhaoDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Xinya GaoDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Lixuan YangDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Jianbo XuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating studies indicate that circular RNAs (circRNAs) play critical roles in cancer progression. Most of them have been reported to act as microRNA sponges or interact with RNA-binding proteins; however, their full range of functions remains largely unclear. Recently, an increasing number of circRNAs have been found to encode proteins. C-E-Cad, a protein encoded by circular E-cadherin (circ-E-Cad), has been shown to have a great influence in the progression of glioblastoma, but its specific role in gastric cancer (GC) is unclear. Here, we found that both circ-E-Cad and C-E-Cad were upregulated in GC cell lines and GC tissues compared with a human gastric epithelial cell line (GES-1) and normal tissues. Knockdown of circ-E-Cad suppressed GC cell line proliferation and metastasis in vitro and in vivo, whereas overexpression of C-E-Cad had the opposite effects. Immunoblotting revealed that C-E-Cad exerted tumor-promoting functions by regulating the PI3K/AKT pathway. A rescue experiment showed that C-E-Cad but not circ-E-Cad was the executor of protumor biological functions. In addition, we demonstrated that the C-E-Cad expression level could have been increased by the TGF-β/Smad pathway. In summary, our results indicated that the TGF-β/Smad pathway could increase the expression of C-E-Cad to regulate GC cell proliferation, migration, and epithelial-mesenchymal transition by affecting PI3K/AKT signaling.

Indexed as

MicroRNAsStomach NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, CircularTransforming Growth Factor betaMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, CircularTransforming Growth Factor betaC-E-CadEMTgastric cancermigrationproliferation

Identifiers

PMID36453704
PMCPMC10107598
OpenAlexW4310566608

What OpenQuestion holds

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Read underepoch 390

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.