Evidence map›Paper›PMID 33291082›Full record

ArticleAging2020

AIM2 inhibits colorectal cancer cell proliferation and migration through suppression of Gli1.

Menglin Xu, Junfeng Wang, Haoran Li, Zhengrong Zhang, Zhengwu Cheng

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
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  8. Article
  9. The Role of the AIM2 Gene in Obesity-Related Glucose and Lipid Metabolic Disorders: A Recent Update.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Inflammasome signaling in colorectal cancer.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
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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 1 institution in 1 country.

Menglin XuDepartment of Oncology, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China.
Junfeng WangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China.
Haoran LiDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China.
Zhengrong ZhangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China.
Zhengwu ChengDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China.
First Affiliated Hospital of Wannan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is a common malignant tumor and is one of the leading causes of cancer-related deaths worldwide. Absent in melanoma 2 (AIM2), as a member of the pyrin-HIN family proteins, plays contentious roles in different types of cancers. In the present work, we provide evidence that AIM2 was commonly downregulated in human CRC and loss of AIM2 significantly correlated with tumor size, depth of invasion, lymph node metastasis (LNM) and TNM (Tumor, Node, Metastases) stage in patients suffering from CRC. AIM2 knockdown promoted CRC cell proliferation, migration and epithelial-mesenchymal transition (EMT) progress, whereas AIM2 overexpression did the opposite. AIM2 inhibited glioma-associated oncogene-1 (Gli1) expression through Smoothened homolog (SMO)-independent pathway and regulated CRC cell proliferation and migration in a Gli1-dependent manner. Moreover, AIM2 could modulate Protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway and the increased Gli1 expression and EMT progress induced by AIM2 depletion was reversed after incubation with AKT inhibitor Ly294002 in CRC cells. In conclusion, our results define AIM2 as a novel regulator of Gli1 in CRC cell growth and metastasis, and suggest that the AIM2/AKT/mTOR/Gli1 signaling axis may serve as a potential target for treatment of CRC.

Indexed as

AdenocarcinomaAgedAnimalsCell Line, TumorCell MovementCell ProliferationChromonesColorectal NeoplasmsDNA-Binding ProteinsEnzyme InhibitorsEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHCT116 CellsHumansLymphatic Metastasis2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAIM2 protein, humanChromonesDNA-Binding ProteinsEnzyme InhibitorsGLI1 protein, humanMorpholinesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesZinc Finger Protein GLI1AIM2colorectal cancerGli1migrationproliferation

Identifiers

PMID33291082
PMCPMC7835022
OpenAlexW3108092296

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.