Evidence map›Paper›PMID 35058503›Full record

ArticleScientific reports2022

RBL2/DREAM-mediated repression of the Aurora kinase A/B pathway determines therapy responsiveness and outcome in p53 WT NSCLC.

Lei Duan, Ricardo E Perez, Sarah Calhoun, Carl G Maki

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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.

Lei DuanDepartment of Anatomy and Cell Biology, Rush University Medical Center, 600 S. Paulina Ave, AcFac 507, Chicago, IL, 60612, USA. Lei_Duan@Rush.edu.
Ricardo E PerezRobert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, IL, USA.
Sarah CalhounDepartment of Anatomy and Cell Biology, Rush University Medical Center, 600 S. Paulina Ave, AcFac 507, Chicago, IL, 60612, USA.
Carl G MakiDepartment of Anatomy and Cell Biology, Rush University Medical Center, 600 S. Paulina Ave, AcFac 507, Chicago, IL, 60612, USA. Carl_Maki@rush.edu.
Rush University Medical Center · USNorthwestern University · US

Funding

Targeting Prolyl Peptidases in Tamoxifen Resistant Breast CancerR01CA200232 · NCI · RUSH UNIVERSITY MEDICAL CENTER · PI MAKI, CARL G · 2016 to 2020
$1.8M
Center for Strategic Scientific Initiatives, National Cancer Institute R01CA200232-05NCI NIH HHS R01 CA200232U.S. Department of Defense 11895064
6 · The paper itself

Abstract

Wild-type p53 is a stress-responsive transcription factor and potent tumor suppressor. P53 activates or represses genes involved in cell cycle progression or apoptosis in order to arrest the cell cycle or induce cell death. Transcription repression by p53 is indirect and requires repressive members of the RB-family (RB1, RBL1, RBL2) and formation of repressor complexes of RB1-E2F and RBL1/RBL2-DREAM. Many aurora kinase A/B (AURKA/B) pathway genes are repressed in a p53-DREAM-dependent manner. We found heightened expression of RBL2 and reduced expression of AURKA/B pathway genes is associated with improved outcomes in p53 wild-type but not p53 mutant non-small cell lung cancer (NSCLC) patients. Knockdown of p53, RBL2, or the DREAM component LIN37 increased AURKA/B pathway gene expression and reduced paclitaxel and radiation toxicity in NSCLC cells. In contrast, pharmacologic inhibition of AURKA/B or knockdown of AURKA/B pathway components increased paclitaxel and IR sensitivity. The results support a model in which p53-RBL2-DREAM-mediated repression of the AURKA/B pathway contributes to tumor suppression, improved tumor therapy responses, and better outcomes in p53 wild-type NSCLCs.

Indexed as

Gene Expression Regulation, NeoplasticAurora Kinase AAurora Kinase BCarcinoma, Non-Small-Cell LungCell Cycle CheckpointsCell Line, TumorHumansPaclitaxelRetinoblastoma-Like Protein p130Tumor Suppressor Protein p53Aurora Kinase AAurora Kinase BPaclitaxelRBL2 protein, humanRetinoblastoma-Like Protein p130Tumor Suppressor Protein p53

Identifiers

PMID35058503
PMCPMC8776870
OpenAlexW4205329919

What OpenQuestion holds

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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.