Evidence map›Paper›PMID 38165468›Full record

ReviewMolecular biology reports2024

The APE1/REF-1 and the hallmarks of cancer.

Priscyanne Barreto Siqueira, Mariana Moreno de Sousa Rodrigues, Ísis Salviano Soares de Amorim, Thayssa Gomes da Silva, Matheus da Silva Oliveira, Juliana Alves Rodrigues, Adenilson de Souza da Fonseca, Andre Luiz Mencalha

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

8 authors at 2 institutions in 1 country.

Priscyanne Barreto Siqueira *Departamento de Biofísica e Biometria, Laboratório de Biologia do Câncer, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil. priscyannebs@gmail.com.ORCID http://orcid.org/0000-0003-2023-6048
Mariana Moreno de Sousa Rodrigues *Departamento de Biofísica e Biometria, Laboratório de Biologia do Câncer, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil. 14morenomariana@gmail.com.ORCID http://orcid.org/0000-0003-0224-7288
Ísis Salviano Soares de AmorimDepartamento de Biofísica e Biometria, Laboratório de Biologia do Câncer, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil.ORCID http://orcid.org/0000-0002-2762-1400
Thayssa Gomes da SilvaDepartamento de Biofísica e Biometria, Laboratório de Biofotônica, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil.ORCID http://orcid.org/0000-0002-0718-1380
Matheus da Silva OliveiraDepartamento de Biofísica e Biometria, Laboratório de Biologia do Câncer, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil.ORCID http://orcid.org/0000-0001-5261-3878
Juliana Alves RodriguesDepartamento de Biofísica e Biometria, Laboratório de Biologia do Câncer, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil.ORCID http://orcid.org/0000-0002-4139-4080
Adenilson de Souza da FonsecaDepartamento de Biofísica e Biometria, Laboratório de Biofotônica, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil.ORCID http://orcid.org/0000-0002-4441-4008
Andre Luiz MencalhaDepartamento de Biofísica e Biometria, Laboratório de Biologia do Câncer, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcântara Gomes, Rio de Janeiro, Brasil.ORCID http://orcid.org/0000-0003-3229-8094
Universidade do Estado do Rio de Janeiro · BRUniversidade Federal do Rio de Janeiro · BR

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 302095/2022-5/CNPqFundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro 200.318/2023/FAPERJ
6 · The paper itself

Abstract

APE1/REF-1 (apurinic/apyrimidinic endonuclease 1 / redox factor-1) is a protein with two domains, with endonuclease function and redox activity. Its main activity described is acting in DNA repair by base excision repair (BER) pathway, which restores DNA damage caused by oxidation, alkylation, and single-strand breaks. In contrast, the APE1 redox domain is responsible for regulating transcription factors, such as AP-1 (activating protein-1), NF-κB (Nuclear Factor kappa B), HIF-1α (Hypoxia-inducible factor 1-alpha), and STAT3 (Signal Transducers and Activators of Transcription 3). These factors are involved in physiological cellular processes, such as cell growth, inflammation, and angiogenesis, as well as in cancer. In human malignant tumors, APE1 overexpression is associated with lung, colon, ovaries, prostate, and breast cancer progression, more aggressive tumor phenotypes, and worse prognosis. In this review, we explore APE1 and its domain's role in cancer development processes, highlighting the role of APE1 in the hallmarks of cancer. We reviewed original articles and reviews from Pubmed related to APE1 and cancer and found that both domains of APE1/REF-1, but mainly its redox activity, are essential to cancer cells. This protein is often overexpressed in cancer, and its expression and activity are correlated to processes such as proliferation, invasion, inflammation, angiogenesis, and resistance to cell death. Therefore, APE1 participates in essential processes of cancer development. Then, the activity of APE1/REF-1 in these hallmarks suggests that targeting this protein could be a good therapeutic approach.

Indexed as

NeoplasmsCell CycleCell DeathEndonucleasesHumansInflammationMaleEndonucleasesAPE1CancerCancer progressionHallmarksTumorigenesis

Identifiers

PMID38165468
OpenAlexW4390501754

What OpenQuestion holds

Textmetadata
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.