Evidence map›Paper›PMID 25301734›Full record

ArticleOncotarget2014

De-acetylation and degradation of HSPA5 is critical for E1A metastasis suppression in breast cancer cells.

Yi-Wen Chang, Hsin-An Chen, Chi-Feng Tseng, Chih-Chen Hong, Jui-Ti Ma, Mien-Chie Hung, Chih-Hsiung Wu, Ming-Te Huang, Jen-Liang Su

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 28% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

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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

9 authors at 6 institutions in 2 countries.

Yi-Wen ChangNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan.
Hsin-An ChenGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Chi-Feng TsengNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan. Graduate Program of Biotechnology in Medicine College of Life Science, National Tsing Hua University, Hsinchu, Taiwan.
Chih-Chen HongNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan.
Jui-Ti MaNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan. Graduate Program of Biotechnology in Medicine College of Life Science, National Tsing Hua University, Hsinchu, Taiwan.
Mien-Chie HungGraduate Institute of Cancer Biology, China Medical University, Taichung, Taiwan. Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan. Department of Biotechnology, Asia University, Taichung, Taiwan. Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Chih-Hsiung WuGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Ming-Te HuangGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan. Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Jen-Liang SuNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan. Graduate Institute of Cancer Biology, China Medical University, Taichung, Taiwan. Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan. Department of Biotechnology, Asia University, Taichung, Taiwan.
National Health Research Institutes · TWTaipei Medical University · TWChina Medical University · TWChina Medical University Hospital · TWNational Tsing Hua University · TWTaipei Medical University-Shuang Ho Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated expression of heat shock protein 5 (HSPA5) promotes drug resistance and metastasis and is a marker of poor prognosis in breast cancer patients. Adenovirus type 5 E1A gene therapy has demonstrated antitumor efficacy but the mechanisms of metastasis-inhibition are unclear. Here, we report that E1A interacts with p300 histone acetyltransferase (HAT) and blocks p300-mediated HSPA5 acetylation at K353, which in turn promotes HSPA5 ubiquitination by GP78 (E3 ubiquitin ligase) and subsequent proteasome-mediated degradation. Our findings point out the Ying-Yang regulation of two different post-translational modifications (ubiquitination and acetylation) of HSPA5 in tumor metastasis.

Indexed as

Cell MovementAcetylationAdenovirus E1A ProteinsAnimalsApoptosisBlotting, WesternBreast NeoplasmsCell ProliferationE1A-Associated p300 ProteinEndoplasmic Reticulum Chaperone BiPFemaleHeat-Shock ProteinsHumansImmunoenzyme TechniquesImmunoprecipitationLung NeoplasmsAdenovirus E1A ProteinsE1A-Associated p300 ProteinEndoplasmic Reticulum Chaperone BiPEP300 protein, humanHeat-Shock ProteinsHSPA5 protein, humanHspa5 protein, mouseRNA, Messenger

Identifiers

PMID25301734
PMCPMC4279393
OpenAlexW1860208758

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.