Evidence map›Paper›PMID 27083003›Full record

ArticleOncotarget2016

Vinca alkaloid drugs promote stress-induced translational repression and stress granule formation.

Witold Szaflarski, Marta M Fay, Nancy Kedersha, Maciej Zabel, Paul Anderson, Pavel Ivanov

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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Connecting the Dots: Stress Granule and Cardiovascular Diseases.Journal of cardiovascular translational research · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Biomolecular condensates and disease pathogenesis.Science China. Life sciences · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
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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

6 authors at 2 institutions in 2 countries.

Witold SzaflarskiDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
Marta M FayDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
Nancy KedershaDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
Maciej ZabelDepartment of Histology and Embryology, Poznan University of Medical Sciences, Poznań, Poland.
Paul AndersonDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
Pavel IvanovDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA, USA.
Harvard University · USPoznan University of Medical Sciences · PL

Funding

Stress granules and cell signalingR01GM111700 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI ANDERSON, PAUL J. · 2014 to 2017
$1.3M
Angiogenin-Induced RNA Cleavage in CancerR01CA168872 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI ANDERSON, PAUL J. · 2013 to 2015
$1.1M
G-quadruplex Structures as Targets and Tools in ALSR21NS094918 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI IVANOV, PAVEL · 2015 to 2016
$488k
NCI NIH HHS R01 CA168872NIGMS NIH HHS R01 GM111700NINDS NIH HHS R21 NS094918
6 · The paper itself

Abstract

Resistance to chemotherapy drugs is a serious therapeutic problem and its underlying molecular mechanisms are complex. Stress granules (SGs), cytoplasmic ribonucleoprotein complexes assembled in cells exposed to stress, are implicated in various aspects of cancer cell metabolism and survival. SGs promote the survival of stressed cells by reprogramming gene expression and inhibiting pro-apoptotic signaling cascades. We show that the vinca alkaloid (VA) class of anti-neoplastic agents potently activates a SG-mediated stress response program. VAs inhibit translation initiation by simultaneous activation of eIF4E-BP1 and phosphorylation of eIF2α, causing polysome disassembly and SG assembly. VA-induced SGs contain canonical SG components but lack specific signaling molecules. Blocking VA-induced SG assembly by inactivating eIF4EBP1 or inhibiting eIF2α phosphorylation decreases cancer cell viability and promotes apoptosis. Our data describe previously unappreciated effects of VAs on cellular RNA metabolism and illuminate the roles of SGs in cancer cell survival.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsCell Line, TumorCells, CulturedCell SurvivalCytoplasmic GranulesEukaryotic Initiation Factor-2HumansMCF-7 CellsMice, KnockoutPhosphorylationProtein BiosynthesisRNA InterferenceStress, PhysiologicalVinca AlkaloidsAntineoplastic AgentsEukaryotic Initiation Factor-2Vinca AlkaloidsVincristinecancerchemotherapystress granulesstress responsetranslation initiation

Identifiers

PMID27083003
PMCPMC5058682
OpenAlexW2339162523

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.