Evidence map›Paper›PMID 27449499›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2017

The Novel KLF4/MSI2 Signaling Pathway Regulates Growth and Metastasis of Pancreatic Cancer.

Kun Guo, Jiujie Cui, Ming Quan, Dacheng Xie, Zhiliang Jia, Daoyan Wei, Liang Wang, Yong Gao, Qingyong Ma, Keping Xie

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 83 citations in OpenAlex.

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  16. [Advances in research of Musashi2 in solid tumors].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 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

10 authors at 3 institutions in 2 countries.

Kun GuoDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Jiujie CuiDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Ming QuanDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Dacheng XieDepartment of Oncology, Shanghai East Hospital, Shanghai Tongji University, Shanghai, P.R. China.
Zhiliang JiaDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Daoyan WeiDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Liang WangDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Yong GaoDepartment of Oncology, Shanghai East Hospital, Shanghai Tongji University, Shanghai, P.R. China. kepxie@mdanderson.org qyma56@xjtu.edu.cn gaoyon@hotmail.com.
Qingyong MaDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China. kepxie@mdanderson.org qyma56@xjtu.edu.cn gaoyon@hotmail.com.
Keping XieDepartment of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas. kepxie@mdanderson.org qyma56@xjtu.edu.cn gaoyon@hotmail.com.
The University of Texas MD Anderson Cancer Center · USShanghai East Hospital · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CN

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
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
Functional Validation of Pancreatic Cancer Progression BiomarkerR01CA152309 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.6M
KLF4 Genetic and Epigenetic Changes in Human Pancreatic CancerR01CA129956 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2008 to 2012
$1.3M
Genetic Approaches to Pancreatic Cancer ProgressionR01CA148954 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2010 to 2014
$1.3M
Molecular basis of pancreatic cancer progression and metastsisR21CA140999 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI XIE, KEPING · 2009 to 2010
$271k
NCI NIH HHS R01 CA129956NCI NIH HHS R01 CA148954NCI NIH HHS R01 CA152309NCI NIH HHS R01 CA172233NCI NIH HHS R01 CA195651NCI NIH HHS R01 CA198090NCI NIH HHS R21 CA140999
6 · The paper itself

Abstract

purposeMusashi 2 (MSI2) is reported to be a potential oncoprotein in cases of leukemia and several solid tumors. However, its expression, function, and regulation in pancreatic ductal adenocarcinoma (PDAC) cases have yet to be demonstrated. Therefore, in the current study, we investigated the clinical significance and biologic effects of MSI2 expression in PDAC cases and sought to delineate the clinical significance of the newly identified Krüppel-like factor 4 (KLF4)/MSI2 regulatory pathway. EXPERIMENTAL

designMSI2 expression and its association with multiple clinicopathologic characteristics in human PDAC specimens were analyzed immunohistochemically. The biological functions of MSI2 regarding PDAC cell growth, migration, invasion, and metastasis were studied using gain- and loss-of-function assays both in vitro and in vivo Regulation of MSI2 expression by KLF4 was examined in several cancer cell lines, and the underlying mechanisms were studied using molecular biologic methods.

resultsMSI2 expression was markedly increased in both PDAC cell lines and human PDAC specimens, and high MSI2 expression was associated with poor prognosis for PDAC. Forced MSI2 expression promoted PDAC proliferation, migration, and invasion in vitro and growth and metastasis in vivo, whereas knockdown of MSI2 expression did the opposite. Transcriptional inhibition of MSI2 expression by KLF4 occurred in multiple PDAC cell lines as well as mouse models of PDAC.

conclusionsLost expression of KLF4, a transcriptional repressor of MSI2 results in overexpression of MSI2 in PDACs, which may be a biomarker for accurate prognosis. A dysregulated KLF4/MSI2 signaling pathway promotes PDAC progression and metastasis. Clin Cancer Res; 23(3); 687-96. ©2016 AACR.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHeterograftsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLiver NeoplasmsMiceMice, NudeNeoplasm MetastasisNeoplasm ProteinsPancreatic NeoplasmsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsMSI2 protein, humanNeoplasm ProteinsRNA-Binding ProteinsRNA, Small Interfering

Identifiers

PMID27449499
PMCPMC5253336
OpenAlexW2476594070

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.