Evidence map›Paper›PMID 29895675›Full record

ArticleCancer research2018

Mcl-1 Phosphorylation without Degradation Mediates Sensitivity to HDAC Inhibitors by Liberating BH3-Only Proteins.

Jingshan Tong, Xingnan Zheng, Xiao Tan, Rochelle Fletcher, Zaneta Nikolovska-Coleska, Jian Yu, Lin Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2018. 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
4.5field-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

45 citing papers in PubMed, 68 citations in OpenAlex.

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  11. Synthetical lethality of Werner helicase and mismatch repair deficiency is mediated by p53 and PUMA in colon cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

7 authors at 1 institution in 1 country.

Jingshan TongUPMC Hillman Cancer Center, Pittsburgh, Pennsylvania.
Xingnan ZhengUPMC Hillman Cancer Center, Pittsburgh, Pennsylvania.
Xiao TanUPMC Hillman Cancer Center, Pittsburgh, Pennsylvania.
Rochelle FletcherUPMC Hillman Cancer Center, Pittsburgh, Pennsylvania.
Zaneta Nikolovska-ColeskaDepartment of Pathology, University of Michigan School of Medicine, Ann Arbor, Michigan.
Jian YuUPMC Hillman Cancer Center, Pittsburgh, Pennsylvania.
Lin ZhangUPMC Hillman Cancer Center, Pittsburgh, Pennsylvania. zhanglx@upmc.edu.
University of Pittsburgh · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JOHN C. BYRD · 1988 to 2026
$158.0M
Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
Novel Mcl-1 inhibitors for overcoming therapeutic resistance in colorectal cancerR01CA217141 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NIKOLOVSKA-COLESKA, ZANETA, ZHANG, LIN · 2017 to 2021
$2.6M
Translation addiction and targeting in colon cancerR01CA215481 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YU, JIAN · 2018 to 2022
$2.3M
Role of Mcl-1 degradation in colorecal cancer therapyR01CA203028 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHANG, LIN · 2016 to 2020
$1.7M
Bid-mediated killing of oncogenic stem cells in chemopreventionR01CA172136 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZHANG, LIN · 2013 to 2017
$1.6M
Novel selective small-molecule inhibitors of Mcl-1 proteinR01CA149442 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NIKOLOVSKA-COLESKA, ZANETA · 2010 to 2014
$1.5M
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA149442NCI NIH HHS R01 CA172136NCI NIH HHS R01 CA203028NCI NIH HHS R01 CA215481NCI NIH HHS R01 CA217141NIAID NIH HHS U19 AI068021
6 · The paper itself

Abstract

Mcl-1, a prosurvival Bcl-2 family protein, is frequently overexpressed in cancer cells and plays a critical role in therapeutic resistance. It is well known that anticancer agents induce phosphorylation of Mcl-1, which promotes its binding to E3 ubiquitin ligases and subsequent proteasomal degradation and apoptosis. However, other functions of Mcl-1 phosphorylation in cancer cell death have not been well characterized. In this study, we show in colon cancer cells that histone deacetylase inhibitors (HDACi) induce GSK3β-dependent Mcl-1 phosphorylation, but not degradation or downregulation. The

Indexed as

Apoptosis Regulatory ProteinsBcl-2-Like Protein 11Cell Line, TumorCell SurvivalColonic NeoplasmsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistone DeacetylasesHumansMyeloid Cell Leukemia Sequence 1 ProteinPhosphorylationProteolysisProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Small Molecule LibrariesApoptosis Regulatory ProteinsBBC3 protein, humanBcl-2-Like Protein 11Histone Deacetylase InhibitorsHistone DeacetylasesMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinPMAIP1 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Small Molecule Libraries

Identifiers

PMID29895675
PMCPMC6298746
OpenAlexW2808615008

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.