Evidence map›Paper›PMID 31870119›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2019

AMPK Activation of Apoptotic Markers in Human Breast Cancer Cell Lines with Different p53 Backgrounds: MCF-7, MDA-MB-231 and T47D Cells.

Omar S El-Masry, Barry L Brown, Pauline R M Dobson

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 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

3 authors at 2 institutions in 2 countries.

Omar S El-MasryDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abulrahman Bin Faisal University, 31441, Dammam, Saudi Arabia.ORCID 0000-0002-0226-2923
Barry L BrownDepartment of Human Metabolism, The Medical School, University of Sheffield, Sheffield, S10 2RX, United Kingdom.
Pauline R M DobsonDepartment of Human Metabolism, The Medical School, University of Sheffield, Sheffield, S10 2RX, United Kingdom.
University of Sheffield · GBImam Abdulrahman Bin Faisal University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDownregulation of AMPK has been established as a major contributor to carcinogenesis in many types of human cancer. We sought to investigate the influence of activated AMPK on apoptotic markers in human breast cancer cells differing in their p53 status, as well as estrogen receptor status (MCF-7 (p53+ and ER+), MDA-MB-231 (p53 mutant and ER-) and T47D (p53 mutant and ER+)).

methodsWe examined the effect of AICAR-activated AMPK on PARP cleavage, Bax redistribution, the involvement of intrinsic and extrinsic pathways of apoptosis using selective caspase inhibitors and cell cycle progression and p21 levels.

resultsPARP cleavage occurred to a greater extent in MCF-7 and MDA-MB-231 cells, whereas Bax translocation was slower in MDA-MB-231 cells. Although there were quantitative differences in the effect of caspase inhibitors, it was clear that AMPK activation predominately affected the intrinsic pathway of apoptosis. Although, p21 was increased in all 3 cell types, there were quantitative and time differences. Apoptosis, as measured by fluorimetry, was increased in all three cell types.

conclusionThe impact of AMPK activation was cell type dependent resulting in differential activation of apoptotic markers, confirming that the genetic background of breast cancer may have an influence on the mode of action of AMPK. Thus, different anti-tumour mechanisms may be elicited depending on the cellular genotype.

Indexed as

ApoptosisGene Expression Regulation, NeoplasticAminoimidazole CarboxamideAMP-Activated Protein Kinasesbcl-2-Associated X ProteinBreast NeoplasmsCell CycleCell ProliferationCyclin-Dependent Kinase Inhibitor p21FemaleHumansHypoglycemic AgentsPoly (ADP-Ribose) Polymerase-1Receptors, EstrogenRibonucleotidesTumor Cells, CulturedAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesBAX protein, humanbcl-2-Associated X ProteinCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Hypoglycemic AgentsPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1Receptors, EstrogenRibonucleotidesTP53 protein, humanTumor Suppressor Protein p53AMPKApoptosisbreast cancerCell cyclePARP

Identifiers

PMID31870119
PMCPMC7173391
OpenAlexW2997954503

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.