Evidence map›Paper›PMID 25695667›Full record

ArticleCancer biology & therapy2015

Heterozygous deletion of ATG5 in Apc(Min/+) mice promotes intestinal adenoma growth and enhances the antitumor efficacy of interferon-gamma.

Lu Wang, Yan Wang, Yuyin Lu, Qianyun Zhang, Xianjun Qu

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The application of ApcJournal of cancer research and clinical oncology · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Autophagy regulation and its role in gastric cancer and colorectal cancer.Cancer biomarkers : section A of Disease markers · 2016
    Review
  17. Review
  18. Autophagy and AML--food for thought.Cell death and differentiation · 2016
    Article
  19. 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

5 authors at 2 institutions in 2 countries.

Lu Wanga Department of Pharmacology; School of Pharmaceutical Sciences ; Shandong University ; Jinan , Shandong , China.
Yan Wang
Yuyin Lu
Qianyun Zhang
Xianjun Qu
Shandong University · CNXinjiang Institute of Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy related gene 5 (ATG5) was lost in 23% of the patients with colorectal cancer (CRC) and the role of loss of ATG5 in the pathogenesis of CRC remains unclear. Knockdown of ATG5 in cancer cells enhances the antitumor efficacy of lots of chemotherapeutic agents. However, there is still no animal model to validate these in vitro observations in vivo. In this study, we found that heterozygous deletion of ATG5 in Apc(Min/+) mice increased the number and size of adenomas as compared with those in Apc(Min/+)ATG5(+/+) mice. To investigate whether ATG5 deficiency could sensitize tumors to chemotherapies, we compared the antitumor effects of Interferon-gamma (IFN-γ) between Apc(Min/+)ATG5(+/+) and Apc(Min/+)ATG5(+/-) mice, as IFN-γ is a potential tumor suppressor for CRC and has been used clinically as an efficient adjuvant to chemotherapy of cancer. We revealed that heterozygous deletion of ATG5 significantly enhanced the antitumor efficacy of IFN-γ. Early treatment of Apc(Min/+)ATG5(+/-) mice with IFN-γ decreased tumor incidence rate to 16.7% and reduced the number of adenomas by 95.5% and late treatment led to regression of tumor. Moreover, IFN-γ treatment did not cause any evident toxic reaction. Mechanistic analysis revealed that heterozygous deletion of ATG5 activated EGFR/ERK1/2 and Wnt/β-catenin pathways in adenomas of Apc(Min/+) mice and enhanced the effects of IFN-γ-dependent inhibition of these 2 pathways. Our results demonstrate that ATG5 plays important roles in intestinal tumor growth and combination of IFN-γ and ATG5 deficiency or ATG5-targeted inhibition is a promising strategy for prevention and treatment of CRC.

Indexed as

AdenomaAdenomatous Polyposis Coli ProteinAnimalsAutophagy-Related Protein 5Cell Transformation, NeoplasticDisease Models, AnimalGene Expression Regulation, NeoplasticHumansInterferon-gammaIntestinal NeoplasmsMiceMicrotubule-Associated ProteinsSequence DeletionAdenomatous Polyposis Coli ProteinAtg5 protein, mouseAutophagy-Related Protein 5Interferon-gammaMicrotubule-Associated Proteins5-FU, 5-fluorouracilApc, adenomatous polyposis coliApcMin/+ mouseATG5ATG5, autophagy related gene 5colorectal cancerCRC, colorectal cancerEGFR, epidermal growth factor receptorErk, extracellular signal-regulated kinaseheterozygous deletionIFN-γIFN-γ, Interferon-gammaintestinal adenomaLC3, microtubule-associated protein 1 light chain 3PCNA, proliferating cell nuclear antigensiRNAs, small interfering RNAs

Identifiers

PMID25695667
PMCPMC4622965
OpenAlexW1820742834

What OpenQuestion holds

Textmetadata
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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.