Evidence map›Paper›PMID 37683260›Full record

ReviewCancer research2023

Targeting the RNA-Binding Protein HuR in Cancer.

Jennifer M Finan, Thomas L Sutton, Dan A Dixon, Jonathan R Brody

Abstract readReview
In one paragraph

Review in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

53 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Macrophage PABPC4-SPP1 Axis Orchestrates Immunosuppression in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. [Metformin Inhibits Prostate Cancer Progression via Regulation of the AKT/mTOR Signaling Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Jennifer M Finan *Department of Surgery, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0001-7706-1643
Thomas L Sutton *Department of Surgery, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0002-2894-7154
Dan A DixonDepartment of Molecular Biosciences, University of Kansas, Lawrence, Kansas.ORCID 0000-0001-5631-4365
Jonathan R BrodyDepartment of Surgery, Oregon Health & Science University, Portland, Oregon.ORCID 0000-0003-3680-3270
Oregon Health & Science University · USUniversity of Kansas · US

Funding

Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
Transgenic & Gene-Targeting Shared ResourceP30CA168524 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOLE L NOLLEN · 2012 to 2026
$40.1M
Nano-Engineered Lab-on-a-Chip for Assessing HuR-Regulated Exosomes for Cancer Monitoring and Targeted TherapyR01CA243445 · NCI · UNIVERSITY OF KANSAS LAWRENCE · PI DIXON, DAN ALAN, XU, LIANG · 2019 to 2023
$3.0M
Comparative analysis between patient-derived models of pancreatic ductal adenocarcinomas and matched tumor specimensU01CA224012 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BRODY, JONATHAN, COUSSENS, LISA M. · 2019 to 2023
$2.9M
Optimizing anti-wild-type IDH1 therapy in pancreatic cancerR01CA287672 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI Jonathan Brody, Jordan M Winter · 2024 to 2026
$2.0M
Targeting HuR to improve a synthetic lethal therapy for pancreatic cancerR01CA212600 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BRODY, JONATHAN · 2017 to 2021
$1.9M
Developing a patient derived model platform to treat BRCA1/2-mutant pancreatic cancersR21CA263996 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BRODY, JONATHAN, SEARS, ROSALIE C · 2022 to 2023
$370k
NCI NIH HHS P30 CA069533NCI NIH HHS P30 CA168524NCI NIH HHS R01 CA212600NCI NIH HHS R01 CA243445NCI NIH HHS R01 CA287672NCI NIH HHS R21 CA263996NCI NIH HHS U01 CA224012
6 · The paper itself

Abstract

The RNA-binding protein human antigen R (HuR) is a well-established regulator of gene expression at the posttranscriptional level. Its dysregulation has been implicated in various human diseases, particularly cancer. In cancer, HuR is considered "active" when it shows increased subcellular localization in the cytoplasm, in addition to its normal nuclear localization. Cytoplasmic HuR plays a crucial role in stabilizing and enhancing the translation of prosurvival mRNAs that are involved in stress responses relevant to cancer progression, such as hypoxia, radiotherapy, and chemotherapy. In general, due to HuR's abundance and function in cancer cells compared with normal cells, it is an appealing target for oncology research. Exploiting the principles underlying HuR's role in tumorigenesis and resistance to stressors, targeting HuR has the potential for synergy with existing and novel oncologic therapies. This review aims to explore HuR's role in homeostasis and cancer pathophysiology, as well as current targeting strategies, which include silencing HuR expression, preventing its translocation and dimerization from the nucleus to the cytoplasm, and inhibiting mRNA binding. Furthermore, this review will discuss recent studies investigating the potential synergy between HuR inhibition and traditional chemotherapeutics.

Indexed as

ELAV-Like Protein 1NeoplasmsELAV ProteinsHumansRNA-Binding ProteinsRNA, MessengerELAV-Like Protein 1ELAV ProteinsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID37683260
PMCPMC13449165
OpenAlexW4386554129

What OpenQuestion holds

Textmetadata
LicenceTDM
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.