Evidence map›Paper›PMID 25985210›Full record

ArticleOncogenesis2015

The oncogenic role of the cochaperone Sgt1.

H Ogi, Y Sakuraba, R Kitagawa, L Xiao, C Shen, M A Cynthia, S Ohta, M A Arnold, N Ramirez, P J Houghton and 1 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Hsp90: A means to an end.Cell stress & chaperones · 2026
    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

11 authors at 2 institutions in 1 country.

H OgiCenter for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
Y SakurabaCenter for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
R KitagawaCenter for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
L XiaoCenter for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
C ShenCenter for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
M A CynthiaDepartment of Pathology and Laboratory Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
S OhtaCenter for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
M A ArnoldDepartment of Pathology and Laboratory Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
N RamirezDepartment of Pathology and Laboratory Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
P J Houghton1] Center for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA [2] Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, OH, USA [3] Children's Cancer Research Institute, San Antonio, TX, USA.
K Kitagawa1] Center for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA [2] Department of Pediatrics, College of Medicine, The Ohio State University, Columbus, OH, USA.
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

XENOGRAFT AND CELL LINE COREP01CA165995 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LONDON, CHERYL A · 2013 to 2017
$7.9M
NCI NIH HHS P01 CA165995
6 · The paper itself

Abstract

Sgt1/Sugt1, a cochaperone of Hsp90, is involved in several cellular activities including Cullin E3 ubiqutin ligase activity. The high level of Sgt1 expression in colorectal and gastric tumors suggests that Sgt1 is involved in tumorigenesis. Here, we report that Sgt1 is overexpressed in colon, breast and lung tumor tissues and in Ewing sarcoma and rhabdomyosarcoma xenografts. We also found that Sgt1 heterozygous knockout resulted in suppressed Hras-mediated transformation in vitro and tumor formation in p53(-/-) mouse embryonic fibroblast cells and significantly increased survival of p53(-/-) mice. Moreover, depletion of Sgt1 inhibited the growth of Ewing sarcoma and rhabdomyosarcoma cells and destabilized EWS-FLI1 and PAX3-FOXO1 oncogenic fusion proteins, respectively, which are required for cellular growth. Our results suggest that Sgt1 contributes to cancer development by stabilizing oncoproteins and that Sgt1 is a potential therapeutic target.

Identifiers

PMID25985210
PMCPMC4450263
OpenAlexW1553327745

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.