Evidence map›Paper›PMID 27283903›Full record

ArticleOncotarget2016

Cancer-secreted AGR2 induces programmed cell death in normal cells.

Elizabeth A Vitello, Sue-Ing Quek, Heather Kincaid, Thomas Fuchs, Daniel J Crichton, Pamela Troisch, Alvin Y Liu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. From development to cancer - an ever-increasing role of AGR2.American journal of cancer research · 2021
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
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

7 authors at 4 institutions in 2 countries.

Elizabeth A VitelloDepartment of Urology and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA, USA.
Sue-Ing QuekDepartment of Urology and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA, USA.
Heather KincaidEDRN Informatics Center and NASA Jet Propulsion Laboratory, Pasadena, CA, USA.
Thomas FuchsEDRN Informatics Center and NASA Jet Propulsion Laboratory, Pasadena, CA, USA.
Daniel J CrichtonEDRN Informatics Center and NASA Jet Propulsion Laboratory, Pasadena, CA, USA.
Pamela TroischInsititute for Systems Biology, Seattle, WA, USA.
Alvin Y LiuDepartment of Urology and Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, WA, USA.
Jet Propulsion Laboratory · USUniversity of Washington · USInstitute for Systems Biology · USSingapore Polytechnic · SG

Funding

The Early Detection Research Network: Biomarker Developmental LaboratoriesU01CA111244 · NCI · UNIVERSITY OF WASHINGTON · PI LIU, ALVIN Y · 2004 to 2015
$4.1M
NCI NIH HHS U01 CA111244
6 · The paper itself

Abstract

Anterior Gradient 2 (AGR2) is a protein expressed in many solid tumor types including prostate, pancreatic, breast and lung. AGR2 functions as a protein disulfide isomerase in the endoplasmic reticulum. However, AGR2 is secreted by cancer cells that overexpress this molecule. Secretion of AGR2 was also found in salamander limb regeneration. Due to its ubiquity, tumor secretion of AGR2 must serve an important role in cancer, yet its molecular function is largely unknown. This study examined the effect of cancer-secreted AGR2 on normal cells. Prostate stromal cells were cultured, and tissue digestion media containing AGR2 prepared from prostate primary cancer 10-076 CP and adenocarcinoma LuCaP 70CR xenograft were added. The control were tissue digestion media containing no AGR2 prepared from benign prostate 10-076 NP and small cell carcinoma LuCaP 145.1 xenograft. In the presence of tumor-secreted AGR2, the stromal cells were found to undergo programmed cell death (PCD) characterized by formation of cellular blebs, cell shrinkage, and DNA fragmentation as seen when the stromal cells were UV irradiated or treated by a pro-apoptotic drug. PCD could be prevented with the addition of the monoclonal AGR2-neutralizing antibody P3A5. DNA microarray analysis of LuCaP 70CR media-treated vs. LuCaP 145.1 media-treated cells showed downregulation of the gene SAT1 as a major change in cells exposed to AGR2. RT-PCR analysis confirmed the array result. SAT1 encodes spermidine/spermine N1-acetyltransferase, which maintains intracellular polyamine levels. Abnormal polyamine metabolism as a result of altered SAT1 activity has an adverse effect on cells through the induction of PCD.

Indexed as

ApoptosisAcetyltransferasesAnimalsBiomarkers, TumorDiamine N-AcetyltransferaseDNA FragmentationGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiceMucoproteinsNeoplasm TransplantationOligonucleotide Array Sequence AnalysisOncogene ProteinsProstateAcetyltransferasesAGR2 protein, humanBiomarkers, TumorDiamine N-AcetyltransferaseMucoproteinsOncogene ProteinsProteinsAGR2programmed cell deathprostate cancer cell typesprostate stromal cellsSAT1

Identifiers

PMID27283903
PMCPMC5226518
OpenAlexW2413178163

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.