Evidence map›Paper›PMID 21830157›Full record

ArticleJournal of cancer research and clinical oncology2011

Molecular mechanisms of A3 adenosine receptor-induced G1 cell cycle arrest and apoptosis in androgen-dependent and independent prostate cancer cell lines: involvement of intrinsic pathway.

Mahmoud Aghaei, Mojtaba Panjehpour, Fatemeh Karami-Tehrani, Siamak Salami

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Adenosine AFEBS open bio · 2025
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  8. Targeting Adenosine Receptor Signaling in Cancer Immunotherapy.International journal of molecular sciences · 2018
    Review
  9. Article
  10. AMedicinal research reviews · 2018
    Review
  11. Article
  12. Article
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  14. Article
  15. Evaluation of RIP1K and RIP3K expressions in the malignant and benign breast tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Article
  17. Mitochondrial and caspase pathways are involved in the induction of apoptosis by IB-MECA in ovarian cancer cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  18. Article
  19. Review
  20. Purinergic signalling and cancer.Purinergic signalling · 2013
    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

4 authors at 3 institutions in 1 country.

Mahmoud AghaeiDepartment of Clinical Biochemistry, Cancer Research Laboratory, School of Medical Science, Tarbiat Modares University, P.O. Box: 14115-331, Tehran, Iran.
Mojtaba Panjehpour
Fatemeh Karami-Tehrani
Siamak Salami
Tarbiat Modares University · IRIsfahan University of Medical Sciences · IRUrmia University of Medical Sciences

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeA3 adenosine receptor has shown several physiological and pathological activities, including cell proliferation and apoptosis in various cancer cell lines. This study is designed to investigate molecular mechanism and apoptotic pathway of A3 adenosine receptor in DU-145, PC3 and LNcap-FGC10 human prostate cancer cells.

methodsThe expression level of A3 adenosine receptor was examined using real-time RT-PCR. cAMP concentration was also measured. MTT viability, cell counting and BrdU incorporation tests were used to study the cell proliferation effect of IB-MECA. Cell cycle analysis, Annexin V-FITC staining, Hoechst 33258 staining, mitochondrial membrane potential (ΔΨM), caspase-3 activity, Bcl-2 and Bax protein expression were used to detect apoptosis.

resultA3 adenosine receptors mRNAs were detected at different levels. IB-MECA inhibited forskolin-stimulated cAMP. IB-MECA at (1 μM) suppressed cell proliferation and induced G1 cell cycle arrest. Indeed, IB-MECA down-regulated the expression of CDK4, cyclin D1 and up-regulated p53 expression. IB-MECA at (10-100 μM) induced apoptosis. The activity of caspase-3 was also increased. Expression of Bcl-2 was decreased in response to IB-MECA, while the expression of Bax protein was increased. The results showed a significant loss of ΔΨM, in a dose-dependent manner.

conclusionThis study introduces a possible mechanism through A3 adenosine receptor activation. IB-MECA inhibited prostate cancer cells proliferation and induced G1 cell cycle arrest through p53, Cdk4/cyclinD1 pathway. Apoptosis determined by characteristic morphological changes and increased in sub-G1 population. Loss of MMP, activation of caspase-3 and down-regulation of Bcl-2 expression indicated mitochondrial signaling pathway that involved in the apoptosis.

Indexed as

ApoptosisG1 PhaseAdenosineCaspase 3Cell Line, TumorCell ProliferationCyclic AMPHumansMaleMembrane Potential, MitochondrialNeoplasms, Hormone-DependentProstatic NeoplasmsReceptor, Adenosine A3Tumor Suppressor Protein p53AdenosineCaspase 3Cyclic AMPN(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosineReceptor, Adenosine A3Tumor Suppressor Protein p53

Identifiers

PMID21830157
PMCPMC11828242
OpenAlexW2027844382

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.