Evidence map›Paper›PMID 27923832›Full record

ArticleCancer research2017

ESE3 Inhibits Pancreatic Cancer Metastasis by Upregulating E-Cadherin.

Tiansuo Zhao, Wenna Jiang, Xiuchao Wang, Hongwei Wang, Chen Zheng, Yang Li, Yan Sun, Chongbiao Huang, Zhi-Bo Han, Shengyu Yang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 66 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

14 authors at 4 institutions in 2 countries.

Tiansuo ZhaoTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Wenna JiangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Xiuchao WangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Hongwei WangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Chen ZhengTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Yang LiTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Yan SunDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, P.R. China.
Chongbiao HuangTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Zhi-Bo HanInstitute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, P.R. China.
Shengyu YangDepartment of Tumor Biology and Comprehensive Melanoma Research Center, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Zhiliang JiaDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Keping XieDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas. kepxie@mdanderson.org haojihui@tjmuch.com renhe@tjmuch.com.
He RenTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China.
Jihui HaoTianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, P.R. China. kepxie@mdanderson.org haojihui@tjmuch.com renhe@tjmuch.com.
Tianjin Medical University Cancer Institute and Hospital · CNThe University of Texas MD Anderson Cancer Center · USChinese Academy of Medical Sciences & Peking Union Medical College · CNMoffitt Cancer Center · US

Funding

Clinical Significance of Pancreatic Cancer Differentiation and DedifferentiationR01CA195651 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WANG, HUAMIN · 2015 to 2021
$1.8M
Integrated Signaling in Pancreatic Cancer ProgressionR01CA198090 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRESALIER, ROBERT S · 2016 to 2021
$1.8M
Store-Operated Calcium Entry in Tumor Invasion and MetastasisR01CA175741 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI YANG, SHENGYU · 2014 to 2018
$1.7M
Molecular Mediators of Pancreatic Cancer Invasion and ProgressionR01CA172233 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRESALIER, ROBERT S · 2013 to 2017
$1.7M
NCI NIH HHS R01 CA172233NCI NIH HHS R01 CA175741NCI NIH HHS R01 CA195651NCI NIH HHS R01 CA198090
6 · The paper itself

Abstract

The ETS family transcription factor ESE3 is a crucial element in differentiation and development programs for many epithelial tissues. Here we report its role as a tumor suppressor in pancreatic cancer. We observed drastically lower ESE3 expression in pancreatic ductal adenocarcinomas (PDAC) compared with adjacent normal pancreatic tissue. Reduced expression of ESE3 in PDAC correlated closely with an increase in lymph node metastasis and vessel invasion and a decrease in relapse-free and overall survival in patients. In functional experiments, downregulating the expression of ESE3 promoted PDAC cell motility and invasiveness along with metastasis in an orthotopic mouse model. Mechanistic studies in PDAC cell lines, the orthotopic mouse model, and human PDAC specimens demonstrated that ESE3 inhibited PDAC metastasis by directly upregulating E-cadherin expression at the level of its transcription. Collectively, our results establish ESE3 as a negative regulator of PDAC progression and metastasis by enforcing E-cadherin upregulation.

Indexed as

AnimalsAntigens, CDAzacitidineCadherinsCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementDecitabineHumansMiceNeoplasm InvasivenessNeoplasm MetastasisPancreatic NeoplasmsPromoter Regions, GeneticTranscription FactorsTumor Suppressor ProteinsAntigens, CDAzacitidineCadherinsCDH1 protein, humanDecitabineEHF protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID27923832
PMCPMC5313376
OpenAlexW2560223739

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.