Evidence map›Paper›PMID 23807417›Full record

ArticleRNA biology2013

HuR is a post-transcriptional regulator of core metabolic enzymes in pancreatic cancer.

Richard A Burkhart, Danielle M Pineda, Saswati N Chand, Carmella Romeo, Eric R Londin, Edward D Karoly, Joseph A Cozzitorto, Isidore Rigoutsos, Charles J Yeo, Jonathan R Brody and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Glucose metabolic phenotype of pancreatic cancer.World journal of gastroenterology · 2016
    Pooled it
  2. Trial
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  7. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
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  19. Article
  20. Complex HuR function in pancreatic cancer cells.Wiley interdisciplinary reviews. RNA · 2018
    Review
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

11 authors at 4 institutions in 1 country.

Richard A BurkhartDepartment of Surgery; Jefferson Pancreas, Biliary and Related Cancer Center; Philadelphia, PA USA.
Danielle M Pineda
Saswati N Chand
Carmella Romeo
Eric R Londin
Edward D Karoly
Joseph A Cozzitorto
Isidore Rigoutsos
Charles J Yeo
Jonathan R Brody
Jordan M Winter
Philadelphia University · USComputational Physics (United States) · USJefferson College · USMetabolon (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cell metabolism differs from normal cells, yet the regulatory mechanisms responsible for these differences are incompletely understood, particularly in response to acute changes in the tumor microenvironment. HuR, an RNA-binding protein, acts under acute stress to regulate core signaling pathways in cancer through post-transcriptional regulation of mRNA targets. We demonstrate that HuR regulates the metabolic phenotype in pancreatic cancer cells and is critical for survival under acute glucose deprivation. Using three pancreatic cancer cell line models, HuR-proficient cells demonstrated superior survival under glucose deprivation when compared with isogenic cells with siRNA-silencing of HuR expression (HuR-deficient cells). We found that HuR-proficient cells utilized less glucose, but produced greater lactate, as compared with HuR-deficient cells. Acute glucose deprivation was found to act as a potent stimulus for HuR translocation from the nucleus to the cytoplasm, where HuR stabilizes its mRNA targets. We performed a gene expression array on ribonucleoprotein-immunoprecipitated mRNAs bound to HuR and identified 11 novel HuR target transcripts that encode enzymes central to glucose metabolism. Three (GPI, PRPS2 and IDH1) were selected for validation studies, and confirmed as bona fide HuR targets. These findings establish HuR as a critical regulator of pancreatic cancer cell metabolism and survival under acute glucose deprivation. Further explorations into HuR's role in cancer cell metabolism should uncover novel therapeutic targets that are critical for cancer cell survival in a metabolically compromised tumor microenvironment.

Indexed as

RNA Processing, Post-TranscriptionalCell Line, TumorCell SurvivalCytokinesELAV ProteinsGene Expression Regulation, NeoplasticGlucoseGlucose-6-Phosphate IsomeraseHumansIsocitrate DehydrogenasePancreatic NeoplasmsProtein TransportReproducibility of ResultsRNA, MessengerStress, PhysiologicalTumor MicroenvironmentCytokinesELAV ProteinsGlucoseGlucose-6-Phosphate IsomeraseGPI protein, humanIDH1 protein, humanIsocitrate DehydrogenaseRNA, Messengercancer metabolismHuRpancreatic cancerpost-transcriptional gene regulation

Identifiers

PMID23807417
PMCPMC3817153
OpenAlexW2047190481

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.