Evidence map›Paper›PMID 31312022›Full record

ArticleOncogene2019

Regulation of the unfolded protein response through ATF4 and FAM129A in prostate cancer.

Nora Pällmann, Marte Livgård, Martina Tesikova, Hatice Zeynep Nenseth, Erman Akkus, Jørgen Sikkeland, Yixin Jin, Dogukan Koc, Omer Faruk Kuzu, Manohar Pradhan and 10 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 71 citations in OpenAlex.

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  19. In silico validation of a new classifier, PCSCGClinical and translational medicine · 2023
    Article
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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

20 authors at 4 institutions in 4 countries.

Nora PällmannDepartment of Biosciences, University of Oslo, Oslo, Norway.
Marte LivgårdDepartment of Biosciences, University of Oslo, Oslo, Norway.
Martina TesikovaDepartment of Biosciences, University of Oslo, Oslo, Norway.
Hatice Zeynep NensethDepartment of Biosciences, University of Oslo, Oslo, Norway.
Erman AkkusDepartment of Biosciences, University of Oslo, Oslo, Norway.
Jørgen SikkelandDepartment of Biosciences, University of Oslo, Oslo, Norway.
Yixin JinDepartment of Biosciences, University of Oslo, Oslo, Norway.
Dogukan KocDepartment of Biosciences, University of Oslo, Oslo, Norway.ORCID http://orcid.org/0000-0002-2309-1051
Omer Faruk KuzuDepartment of Biosciences, University of Oslo, Oslo, Norway.
Manohar PradhanInstitute for Cancer Genetics and Informatics, Oslo University Hospital, Oslo, Norway.
Håvard E DanielsenInstitute for Cancer Genetics and Informatics, Oslo University Hospital, Oslo, Norway.
Nermin KahramanDepartment of Experimental Therapeutics, MD Anderson Cancer Center, Houston, TX, USA.
Hamada M MokhlisDepartment of Experimental Therapeutics, MD Anderson Cancer Center, Houston, TX, USA.
Bulent OzpolatDepartment of Experimental Therapeutics, MD Anderson Cancer Center, Houston, TX, USA.
Partha P BanerjeeLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Aykut UrenLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Ladan FazliThe Vancouver Prostate Centre, Vancouver, BC, Canada.
Paul S RennieThe Vancouver Prostate Centre, Vancouver, BC, Canada.
Yang JinDepartment of Biosciences, University of Oslo, Oslo, Norway.
Fahri SaatciogluDepartment of Biosciences, University of Oslo, Oslo, Norway. fahris@ibv.uio.no.
Oslo University Hospital · NOUniversity of Oslo · NOThe University of Texas MD Anderson Cancer Center · USGeorgetown University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells exploit many of the cellular adaptive responses to support their survival needs. One such critical pathway in eukaryotic cells is the unfolded protein response (UPR) that is important in normal physiology as well as disease states, including cancer. Since UPR can serve as a lever between survival and death, regulated control of its activity is critical for tumor formation and growth although the underlying mechanisms are poorly understood. Here we show that one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and survival. Using systemic unbiased gene expression and proteomic analyses, we identified a novel direct ATF4 target gene, family with sequence similarity 129 member A (FAM129A), which is critical in mediating ATF4 effects on prostate tumorigenesis. Interestingly, FAM129A regulated both PERK and eIF2α in a feedback loop that differentially channeled the UPR output. ATF4 and FAM129A protein expression is increased in patient PCa samples compared with benign prostate. Importantly, in vivo therapeutic silencing of ATF4-FAM129A axis profoundly inhibited tumor growth in a preclinical PCa model. These data support that one of the canonical UPR branches, through ATF4 and its target gene FAM129A, is required for PCa growth and thus may serve as a novel therapeutic target.

Indexed as

Activating Transcription Factor 4AnimalsApoptosis Regulatory ProteinsBiomarkers, TumorCell ProliferationEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticHEK293 CellsHumansMaleMiceNeoplasm ProteinsProstatic NeoplasmsSignal TransductionTumor Cells, CulturedUnfolded Protein ResponseActivating Transcription Factor 4Apoptosis Regulatory ProteinsATF4 protein, humanBiomarkers, TumorNeoplasm ProteinsNIBAN1 protein, human

Identifiers

PMID31312022
OpenAlexW2959715062

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.