Evidence map›Paper›PMID 35781781›Full record

ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2022

AMPK's double-faced role in advanced stages of prostate cancer.

Faeze Gharibpoor, Sara Kamali Zonouzi, Sepideh Razi, Nima Rezaei

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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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

4 authors at 3 institutions in 1 country.

Faeze GharibpoorStudent Research Committee, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
Sara Kamali ZonouziCancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Sepideh RaziCancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Nima RezaeiResearch Centre for Immunodeficiencies, Children's Medical Centre, Tehran University of Medical Sciences, Dr. Qarib St, Keshavarz Blvd, Tehran, 14194, Iran. rezaei_nima@tums.ac.ir.ORCID http://orcid.org/0000-0002-3836-1827
Universal Scientific Education and Research Network · IRGuilan University of Medical Sciences · IRIran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is the second leading cause of cancer deaths in men. Unfortunately, a very limited number of drugs are available for the relapsed and advanced stages of PCa, adding only a few months to survival; therefore, it is vital to develop new drugs. 5´ AMP-activated protein kinase (AMPK) is a master regulator of cell metabolism. It plays a significant role in the metabolism of PCa; hence, it can serve well as a treatment option for the advanced stages of PCa. However, whether this pathway contributes to cancer cell survival or death remains unknown. The present study reviews the possible pathways by which AMPK plays role in the advanced stages of PCa, drug resistance, and metastasis: (1) AMPK has a contradictory role in promoting glycolysis and the Warburg effect which are correlated with cancer stem cells (CSCs) survival and advanced PCa. It exerts its effect by interacting with hypoxia-induced factor 1 (HIF1) α, pyruvate kinase 2 (PKM2), glucose transporter (GLUT) 1 and pyruvate dehydrogenase complex (PDHC), which are key regulators of glycolysis; however, whether it promotes or discourage glycolysis is not conclusive. It can also exert an anti-CSC effect by negative regulation of NANOG and epithelial-mesenchymal transition (EMT) transcription factors, which are the major drivers of CSC maintenance; (2) the regulatory effect of AMPK on autophagy is also noticeable. Androgen receptors' expression increases AMPK activation through Calcium/calmodulin-dependent protein kinase 2 (CaMKK2) and induces autophagy. In addition, AMPK itself increases autophagy by downregulating the mammalian target of rapamycin complex (mTORC). However, whether increased autophagy inhibits or promotes cell death and drug resistance is contradictory. This study reveals that there are numerous pathways other than cell metabolism by which AMPK exerts its effects in the advanced stages of PCa, making it a priceless treatment target. Finally, we mention some drugs developed to treat the advanced stages of PCa by acting on AMPK.

Indexed as

AMP-Activated Protein KinasesProstatic NeoplasmsAutophagyCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseGlucose Transport Proteins, FacilitativeHumansMalePyruvate Dehydrogenase ComplexPyruvate KinaseReceptors, AndrogenSignal TransductionTOR Serine-Threonine KinasesTranscription FactorsAMP-Activated Protein KinasesCalciumCalcium-Calmodulin-Dependent Protein Kinase KinaseCAMKK2 protein, humanGlucose Transport Proteins, FacilitativePyruvate Dehydrogenase ComplexPyruvate KinaseReceptors, AndrogenTOR Serine-Threonine KinasesTranscription FactorsAMPKAutophagyCancer stem cellProstate cancerWarburg

Identifiers

PMID35781781
OpenAlexW4283799116

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.