Evidence map›Paper›PMID 35805104›Full record

ReviewCells2022

cAMP Signaling in Cancer: A PKA-CREB and EPAC-Centric Approach.

Muhammad Bilal Ahmed, Abdullah A A Alghamdi, Salman Ul Islam, Joon-Seok Lee, Young-Sup Lee

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
16.4field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Article
  3. A Sesquiterpenoid fromInternational journal of molecular sciences · 2026
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  8. Article
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  10. Protein Expression Status ofLife (Basel, Switzerland) · 2026
    Article
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  13. Review
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  17. Article
  18. Adenosine/AmBio · 2026
    Article
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Muhammad Bilal AhmedBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea.
Abdullah A A AlghamdiDepartment of Biology, Faculty of Science, Albaha University, Albaha 65779, Saudi Arabia.ORCID 0000-0003-3136-9081
Salman Ul IslamDepartment of Pharmacy, Cecos University, Peshawar, Street 1, Sector F 5 Phase 6 Hayatabad, Peshawar 25000, Pakistan.
Joon-Seok LeeBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea.
Young-Sup LeeBK21 FOUR KNU Creative BioResearch Group, School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, Korea.ORCID 0000-0002-5841-6506
Kyungpook National University · KRAl Baha University · SACECOS University · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is one of the most common causes of death globally. Despite extensive research and considerable advances in cancer therapy, the fundamentals of the disease remain unclear. Understanding the key signaling mechanisms that cause cancer cell malignancy may help to uncover new pharmaco-targets. Cyclic adenosine monophosphate (cAMP) regulates various biological functions, including those in malignant cells. Understanding intracellular second messenger pathways is crucial for identifying downstream proteins involved in cancer growth and development. cAMP regulates cell signaling and a variety of physiological and pathological activities. There may be an impact on gene transcription from protein kinase A (PKA) as well as its downstream effectors, such as cAMP response element-binding protein (CREB). The position of CREB downstream of numerous growth signaling pathways implies its oncogenic potential in tumor cells. Tumor growth is associated with increased CREB expression and activation. PKA can be used as both an onco-drug target and a biomarker to find, identify, and stage tumors. Exploring cAMP effectors and their downstream pathways in cancer has become easier using exchange protein directly activated by cAMP (EPAC) modulators. This signaling system may inhibit or accelerate tumor growth depending on the tumor and its environment. As cAMP and its effectors are critical for cancer development, targeting them may be a useful cancer treatment strategy. Moreover, by reviewing the material from a distinct viewpoint, this review aims to give a knowledge of the impact of the cAMP signaling pathway and the related effectors on cancer incidence and development. These innovative insights seek to encourage the development of novel treatment techniques and new approaches.

Indexed as

Cyclic AMP-Dependent Protein KinasesNeoplasmsCREB-Binding ProteinCyclic AMPGuanine Nucleotide Exchange FactorsHumansSignal TransductionCREB-Binding ProteinCyclic AMPCyclic AMP-Dependent Protein KinasesGuanine Nucleotide Exchange FactorscAMPCREBEPACPKAtumor cell

Identifiers

PMID35805104
PMCPMC9266045
OpenAlexW4283455081

What OpenQuestion 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 OpenQuestion graph.