Evidence map›Paper›PMID 32899451›Full record

ReviewInternational journal of molecular sciences2020

The Role of Epac in Cancer Progression.

Nadine Wehbe, Hasan Slika, Joelle Mesmar, Suzanne A Nasser, Gianfranco Pintus, Serine Baydoun, Adnan Badran, Firas Kobeissy, Ali H Eid, Elias Baydoun

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. 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
3.8field-weighted citation impact, top 6% 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, 38 citations in OpenAlex.

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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

10 authors at 4 institutions in 4 countries.

Nadine WehbeDepartment of Biology, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon.
Hasan SlikaDepartment of Pharmacology and Therapeutics, Faculty of Medicine, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon.
Joelle MesmarDepartment of Biology, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon.
Suzanne A NasserDepartment of Pharmacology, Beirut Arab University, P.O. Box 11-5020 Beirut, Lebanon.ORCID 0000-0002-1655-9832
Gianfranco PintusDepartment of Biomedical Sciences, University of Sharjah, P.O. Box 27272 Sharjah, UAE.ORCID 0000-0002-3031-7733
Serine BaydounDepartment of Radiology, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon.
Adnan BadranDepartment of Basic Sciences, University of Petra, P.O. Box 961343, Amman 11196, Jordan.
Firas KobeissyDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, P.O. Box 11-0236, Beirut, Lebanon.ORCID 0000-0002-5008-6944
Ali H EidDepartment of Pharmacology and Therapeutics, Faculty of Medicine, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon.
Elias BaydounDepartment of Biology, American University of Beirut, P.O. Box 11-0236 Beirut, Lebanon.
American University of Beirut · LBBeirut Arab University · LBPetra University · JOUniversity of Sassari · IT

Funding

American University of Beirut MPP 320133University of Petra 5/4/2020
6 · The paper itself

Abstract

Cancer continues to be a prime contributor to global mortality. Despite tremendous research efforts and major advances in cancer therapy, much remains to be learned about the underlying molecular mechanisms of this debilitating disease. A better understanding of the key signaling events driving the malignant phenotype of cancer cells may help identify new pharmaco-targets. Cyclic adenosine 3',5'-monophosphate (cAMP) modulates a plethora of biological processes, including those that are characteristic of malignant cells. Over the years, most cAMP-mediated actions were attributed to the activity of its effector protein kinase A (PKA). However, studies have revealed an important role for the exchange protein activated by cAMP (Epac) as another effector mediating the actions of cAMP. In cancer, Epac appears to have a dual role in regulating cellular processes that are essential for carcinogenesis. In addition, the development of Epac modulators offered new routes to further explore the role of this cAMP effector and its downstream pathways in cancer. In this review, the potentials of Epac as an attractive target in the fight against cancer are depicted. Additionally, the role of Epac in cancer progression, namely its effect on cancer cell proliferation, migration/metastasis, and apoptosis, with the possible interaction of reactive oxygen species (ROS) in these phenomena, is discussed with emphasis on the underlying mechanisms and pathways.

Indexed as

ApoptosisCell ProliferationCyclic AMPCyclic AMP-Dependent Protein KinasesDisease ProgressionGuanine Nucleotide Exchange FactorsHumansNeoplasmsrap1 GTP-Binding ProteinsSignal TransductionCyclic AMPCyclic AMP-Dependent Protein KinasesGuanine Nucleotide Exchange Factorsrap1 GTP-Binding ProteinsRAPGEF3 protein, humancAMPcancerEpacPKAreactive oxygen species (ROS)

Identifiers

PMID32899451
PMCPMC7555121
OpenAlexW3083571678

What Socratic 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 Socratic graph.