Evidence map›Paper›PMID 25277185›Full record

ArticleOncotarget2014

High mobility group Box-1 inhibits cancer cell motility and metastasis by suppressing activation of transcription factor CREB and nWASP expression.

Zhenghong Zuo, Xun Che, Yulei Wang, Bowen Li, Jingxia Li, Wei Dai, Charles P Lin, Chuanshu Huang

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Role of high-mobility group box 1 in cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
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  10. PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
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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

8 authors at 3 institutions in 2 countries.

Zhenghong ZuoNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY. State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.+ Contributed equally to this work.
Xun CheNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY. Contributed equally to this work.
Yulei WangNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY.
Bowen LiState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Jingxia LiNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY.
Wei DaiNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY.
Charles P LinMouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, MD, USA.
Chuanshu HuangNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY.
New York University · USXiamen University · CNNational Cancer Institute · US

Funding

Vascular Biology SectionZIABC011390 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LIN, PENGNIAN · 2011 to 2020
$15.4M
Reagent/Service CoreP01CA165980 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TANG, ERIC MOON-SHONG M. · 2013 to 2023
$13.5M
Molecular Mechanisms of Nickel-Induced TumorigenicityR01CA112557 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2016
$2.9M
Mechanisms underlying therapeutic effect of a new compound Isorhapontigenin (ISO)R01CA177665 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2013 to 2018
$1.7M
NCI NIH HHS CA112557NCI NIH HHS CA165980NCI NIH HHS CA177665NCI NIH HHS P01 CA165980NCI NIH HHS R01 CA112557NCI NIH HHS R01 CA177665
6 · The paper itself

Abstract

The ability to metastasize is a hallmark of malignant tumors, and metastasis is the principal cause of death of cancer patients. The High Mobility Group Box-1 (HMGB1) is a multifunction protein that serves as both a chromatin protein and an extracellular signaling molecule. Our current study demonstrated a novel mechanism of HMGB1 in the regulation of cancer cell actin polymerization, cell skeleton formation, cancer cell motility and metastasis. We found that knockdown of HMGB1 in human lung cancer A549 cells significantly increased cell β-actin polymerization, cell skeleton formation, cancer cell migration and invasion in vitro, as well as metastasis in vivo. And this increase could be inhibited by treatment of HMGB1 knockdown cells with recombinant human HMGB1. Further studies discovered that HMGB1 suppressed phosphorylation, nuclear translocation, and activation of CREB, by inhibiting nuclear translocation of PKA catalytic subunit. This reduces nWASP mRNA transcription and expression, further impairing cancer cell motility. Our findings on the novel mechanism underlying the HMGB1 anti-metastatic effect on cancer provides significant insight into the understanding of the nature of HMGB1 in cancer invasion and metastasis, further serving as key information for utilization of HMGB1 and its regulated downstream components as new targets for cancer therapy.

Indexed as

Cell MovementAdenocarcinomaAnimalsBlotting, WesternCell Line, TumorCyclic AMP Response Element-Binding ProteinElectrophoretic Mobility Shift AssayFemaleFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHeterograftsHMGB1 ProteinHumansLung NeoplasmsMiceMice, NudeCREB1 protein, humanCyclic AMP Response Element-Binding ProteinHMGB1 ProteinHMGB1 protein, humanWAS protein, humanWiskott-Aldrich Syndrome Protein

Identifiers

PMID25277185
PMCPMC4202136
OpenAlexW2157194785

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.