Evidence map›Paper›PMID 29230015›Full record

ArticleNature cell biology2018

A PERK-miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival.

Yiwen Bu, Akihiro Yoshida, Nilesh Chitnis, Brian J Altman, Feven Tameire, Amanda Oran, Victoria Gennaro, Kent E Armeson, Steven B McMahon, Gerald B Wertheim and 5 more

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
6.7field-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

73 citing papers in PubMed, 106 citations in OpenAlex.

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  19. Major roles of the circadian clock in cancer.Cancer biology & medicine · 2023
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13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 1 country.

Yiwen BuDepartment of Biochemistry and Molecular Biology and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
Akihiro YoshidaDepartment of Biochemistry and Molecular Biology and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
Nilesh ChitnisDepartment of Biochemistry and Molecular Biology and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
Brian J AltmanAbramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Pennsylvania, PA, USA.ORCID 0000-0002-3954-4916
Feven TameireDepartment of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Amanda OranDepartment of Cancer Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.
Victoria GennaroDepartment of Cancer Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.
Kent E ArmesonDepartment of Public Health Sciences and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
Steven B McMahonDepartment of Cancer Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.
Gerald B WertheimDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Chi V DangAbramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Pennsylvania, PA, USA.
Davide RuggeroDepartments of Urology and Cellular and Molecular Pharmacology, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA.
Constantinos KoumenisDepartment of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Serge Y FuchsDepartment of Biomedical Sciences, School of Veterinary Medicine, Philadelphia, PA, USA.
J Alan DiehlDepartment of Biochemistry and Molecular Biology and Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA. diehl@musc.edu.ORCID 0000-0001-9854-5049
Medical University of South Carolina · USUniversity of Pennsylvania · USThomas Jefferson University · USChildren's Hospital of Philadelphia · USPhiladelphia University · USUniversity of California, San Francisco · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
UPR, interferon signaling and tumorigenesisP01CA165997 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2013 to 2023
$10.9M
C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSR01CA057341 · NCI · WISTAR INSTITUTE · PI DANG, CHI V. · 1992 to 2021
$8.3M
MYC--TRANSCRIPTION AND INTERACTION WITH P107R01CA051497 · NCI · WISTAR INSTITUTE · PI DANG, CHI V. · 1995 to 2025
$5.3M
The role of deregulated protein synthesis control in Myc-induced tumorigenesisR01CA140456 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2009 to 2019
$3.3M
Oncogenic Disruption of the Circadian Metabolic Cycle in CancerK99CA204593 · NCI · WISTAR INSTITUTE · PI ALTMAN, BRIAN JAMES · 2016 to 2017
$173k
NCI NIH HHS K99 CA204593NCI NIH HHS P01 CA165997NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA051497NCI NIH HHS R01 CA057341NCI NIH HHS R01 CA140456
6 · The paper itself

Abstract

The unfolded protein response (UPR) is a stress-activated signalling pathway that regulates cell proliferation, metabolism and survival. The circadian clock coordinates metabolism and signal transduction with light/dark cycles. We explore how UPR signalling interfaces with the circadian clock. UPR activation induces a 10 h phase shift in circadian oscillations through induction of miR-211, a PERK-inducible microRNA that transiently suppresses both Bmal1 and Clock, core circadian regulators. Molecular investigation reveals that miR-211 directly regulates Bmal1 and Clock via distinct mechanisms. Suppression of Bmal1 and Clock has the anticipated impact on expression of select circadian genes, but we also find that repression of Bmal1 is essential for UPR-dependent inhibition of protein synthesis and cell adaptation to stresses that disrupt endoplasmic reticulum homeostasis. Our data demonstrate that c-Myc-dependent activation of the UPR inhibits Bmal1 in Burkitt's lymphoma, thereby suppressing both circadian oscillation and ongoing protein synthesis to facilitate tumour progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsARNTL Transcription FactorsB-LymphocytesBone NeoplasmsCell Line, TumorCell SurvivalCircadian ClocksCLOCK ProteinseIF-2 KinaseHeterograftsHumansLight Signal TransductionMaleMiceMice, Inbred C57BLARNTL Transcription FactorsBMAL1 protein, humanCLOCK protein, humanCLOCK ProteinsEIF2AK3 protein, humaneIF-2 KinaseMicroRNAsMIRN211 microRNA, humanRNA, Small Interfering

Identifiers

PMID29230015
PMCPMC5741512
OpenAlexW2773188027

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.