Evidence map›Paper›PMID 38783530›Full record

ArticleCurrent gene therapy2024

AEG-1 as a Novel Therapeutic Target in Colon Cancer: A Study from Silencing AEG-1 in BALB/c Mice to Large Data Analysis.

Sushmitha Sriramulu, Sarubala Malayaperumal, Antara Banerjee, Muralidharan Anbalagan, Makalakshmi Murali Kumar, Rajesh Kanna Nandagopal Radha, Xingyi Liu, Hong Zhang, Guang Hu, Xiao-Feng Sun and 1 more

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In one paragraph

Article in Current gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
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  8. Current medicinal chemistry · 2026
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  14. Article
  15. CD82-associated exhausted CD8Frontiers in immunology · 2025
    Article
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

11 authors.

Sushmitha SriramuluDepartment of Medical Biotechnology, Faculty of Allied Health Sciences, Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI), Kelambakkam, Chennai 603103, India.
Sarubala MalayaperumalDepartment of Medical Biotechnology, Faculty of Allied Health Sciences, Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI), Kelambakkam, Chennai 603103, India.
Antara BanerjeeDepartment of Medical Biotechnology, Faculty of Allied Health Sciences, Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI), Kelambakkam, Chennai 603103, India.
Muralidharan AnbalaganDepartment of Structural and Cellular Biology, Tulane University School of Medicine, New Orleans, LA, USA.
Makalakshmi Murali KumarDepartment of Medical Biotechnology, Faculty of Allied Health Sciences, Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI), Kelambakkam, Chennai 603103, India.
Rajesh Kanna Nandagopal RadhaDepartment of Pathology, Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI), Kelambakkam, Chennai 603103, India.
Xingyi LiuCenter for Systems Biology, Department of Bioinformatics, School of Basic Medicine and Biological Sciences, Suzhou, China.
Hong ZhangSchool of Medicine, Institute of Medical Sciences, Orebro University, SE-701 82 Orebro, Sweden.
Guang HuSchool of Medicine, Institute of Medical Sciences, Orebro University, SE-701 82 Orebro, Sweden.
Xiao-Feng SunDepartment of Oncology and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Surajit PathakDepartment of Medical Biotechnology, Faculty of Allied Health Sciences, Chettinad Academy of Research and Education (CARE), Chettinad Hospital and Research Institute (CHRI), Kelambakkam, Chennai 603103, India.

Funding

Department of Science and Technology (DST)-Science and Engineering Research Board (SERB) EMR/2017/001877
6 · The paper itself

Abstract

backgroundAstrocyte elevated gene-1 (AEG-1) is overexpressed in various malignancies. Exostosin-1 (EXT-1), a tumor suppressor, is an intermediate for malignant tumors. Understanding the mechanism behind the interaction between AEG-1 and EXT-1 may provide insights into colon cancer metastasis.

methodsAOM/DSS was used to induce tumor in BALB/c mice. Using an

resultsIn BALB/c mice, the AOM+DSS treated mice developed necrotic, inflammatory and dysplastic changes in the colon with definite clinical symptoms such as loss of goblet cells, colon shortening, and collagen deposition. Administration of AEG-1 siRNA resulted in a substantial decrease in the disease activity index. Mice treated with EXT-1 siRNA showed diffusely reduced goblet cells. In vivo investigations revealed that PTCH-1 activity was influenced by upstream gene AEG-1, which in turn may affect EXT-1 activity. Data from The Cancer Genomic Atlas and GEO databases confirmed the upregulation of AEG-1 and downregulation of EXT-1 in cancer patients.

conclusionsThis study revealed that AEG-1 silencing might alter EXT-1 expression indirectly through PTCH-1, influencing cell-ECM interactions, and decreasing dysplastic changes, proliferation and invasion.

Indexed as

Colonic NeoplasmsMembrane ProteinsMice, Inbred BALB CRNA-Binding ProteinsRNA, Small InterferingAnimalsCell Adhesion MoleculesCell Line, TumorGene Expression Regulation, NeoplasticGene SilencingHumansMaleMiceCell Adhesion MoleculesMembrane ProteinsMtdh protein, mouseRNA-Binding ProteinsRNA, Small InterferingAEG-1BALB/C mice.colon cancerEXT-1GEOTCGA

Identifiers

PMID38783530

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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.