Evidence map›Paper›PMID 32266066›Full record

ArticleCancer & metabolism2020

Metabolic regulation of calcium pumps in pancreatic cancer: role of phosphofructokinase-fructose-bisphosphatase-3 (PFKFB3).

D A Richardson, P Sritangos, A D James, A Sultan, J I E Bruce

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer & metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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  19. CaCancers · 2021
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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

5 authors at 2 institutions in 1 country.

D A Richardson1Division of Cancer Sciences, School of Medical Sciences, University Of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT UK.
P Sritangos1Division of Cancer Sciences, School of Medical Sciences, University Of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT UK.
A D James2Department of Biology, University of York, Heslington, York, UK.
A Sultan1Division of Cancer Sciences, School of Medical Sciences, University Of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT UK.
J I E Bruce1Division of Cancer Sciences, School of Medical Sciences, University Of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT UK.
University of Manchester · GBUniversity of York · GB

Funding

Medical Research Council MR/P00251X/1
6 · The paper itself

Abstract

backgroundHigh glycolytic rate is a hallmark of cancer (Warburg effect). Glycolytic ATP is required for fuelling plasma membrane calcium ATPases (PMCAs), responsible for extrusion of cytosolic calcium, in pancreatic ductal adenocarcinoma (PDAC). Phosphofructokinase-fructose-bisphosphatase-3 (PFKFB3) is a glycolytic driver that activates key rate-limiting enzyme Phosphofructokinase-1; we investigated whether PFKFB3 is required for PMCA function in PDAC cells.

methodsPDAC cell-lines, MIA PaCa-2, BxPC-3, PANC1 and non-cancerous human pancreatic stellate cells (HPSCs) were used. Cell growth, death and metabolism were assessed using sulforhodamine-B/tetrazolium-based assays, poly-ADP-ribose-polymerase (PARP1) cleavage and seahorse XF analysis, respectively. ATP was measured using a luciferase-based assay, membrane proteins were isolated using a kit and intracellular calcium concentration and PMCA activity were measured using Fura-2 fluorescence imaging.

resultsPFKFB3 was highly expressed in PDAC cells but not HPSCs. In MIA PaCa-2, a pool of PFKFB3 was identified at the plasma membrane. PFKFB3 inhibitor, PFK15, caused reduced cell growth and PMCA activity, leading to calcium overload and apoptosis in PDAC cells. PFK15 reduced glycolysis but had no effect on steady-state ATP concentration in MIA PaCa-2.

conclusionsPFKFB3 is important for maintaining PMCA function in PDAC, independently of cytosolic ATP levels and may be involved in providing a localised ATP supply at the plasma membrane.

Indexed as

Calcium overloadCalcium pumpsGlycolysisMetabolismPancreatic cancerPDACPFKFB3PMCA

Identifiers

PMID32266066
PMCPMC7114799
OpenAlexW3005033033

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.