Evidence map›Paper›PMID 27802207›Full record

ArticleCancer biomarkers : section A of Disease markers2016

APE1 overexpression promotes the progression of ovarian cancer and serves as a potential therapeutic target.

Xuemei Wen, Renquan Lu, Suhong Xie, Hui Zheng, Hongling Wang, Yanchun Wang, Jiajun Sun, Xiang Gao, Lin Guo

Abstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024
    Review
  9. The inhibitor of the redox activity of APE1/REF-1, APX2009, reduces the malignant phenotype of breast cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Xuemei WenDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Renquan LuDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Suhong XieDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Hui ZhengDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Hongling WangDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Yanchun WangDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Jiajun SunDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Xiang GaoDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Lin GuoDepartment of Clinical Laboratory, Fudan University Shanghai Cancer Center, Shanghai, China.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme that is involved in DNA repair and the redox regulation of transcription factors. Blocking these functions leads to cell-growth inhibition, apoptosis and other effects. Previous studies have demonstrated that high expression levels of the APE1 protein are associated with the progression and chemoresistance of cancers. We hypothesized that APE1 silencing in ovarian cancer cells might have anticancer effects mediated by cell-growth inhibition and an increase in drug-sensitivity.

objectiveIn this study, we explored the consequences of APE1 silencing in ovarian cancer cells.

methodsImmunohistochemistry (IHC) was used to detect the APE1 protein levels in tissue samples from twelve ovarian cancer (OC) patients and eleven non-OC patients. APE1 knockdown was achieved via the stable transfection of SKOV3 and A2780 cells with a construct encoding a short hairpin DNA directed against the APE1 gene. Then, cell proliferation, colony formation, cell cycle and apoptosis assays were performed to reveal the consequences of APE1 silencing in ovarian cancer cells. Additionally, the SKOV3 and A2780 cells were subjected to the treatment with camptothecin (CPT) and ultraviolet rays (UV) to assess the possible link between the APE1 protein and drug-resistance.

resultsOur results revealed that the APE1 protein was overexpressed in OC tissues. APE1 knockdown in A2780 and SKOV3 cells reduced cell proliferation, arrested cell cycle progression, repressed colony formation and weakly promoted cell apoptosis through the BAX and BCL-2 apoptotic pathways. Additionally, the down-regulation of APE1 significantly enhanced the sensitivity of ovarian cancer cells to the CPT/UV treatment.

conclusionOur study suggested that the APE1 protein is important for the proliferation and growth of ovarian cancer cells. APE1 silencing might enhance drug-sensitivity, and thus APE1 might serve as a novel anti-OC therapeutic target.

Indexed as

Gene ExpressionApoptosisCell CycleCell Line, TumorCell ProliferationDisease ProgressionDNA-(Apurinic or Apyrimidinic Site) LyaseFemaleGene Knockdown TechniquesHistonesHumansOvarian NeoplasmsRNA InterferenceRNA, MessengerRNA, Small InterferingAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseHistonesRNA, MessengerRNA, Small InterferingapoptosisApurinic/apyrimidinic endonuclease 1ovarian cancerproliferation

Identifiers

PMID27802207
PMCPMC13020497
OpenAlexW2475259948

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.