Evidence map›Paper›PMID 28659634›Full record

ArticleScientific reports2017

DACH1 suppresses breast cancer as a negative regulator of CD44.

Hanxiao Xu, Shengnan Yu, Xun Yuan, Jing Xiong, Dong Kuang, Richard G Pestell, Kongming Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

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  20. RDGN-based predictive model for the prognosis of breast cancer.Experimental hematology & oncology · 2020
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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

7 authors at 2 institutions in 2 countries.

Hanxiao XuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Shengnan YuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xun YuanDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jing XiongDepartment of Pathology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Dong KuangDepartment of Pathology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Richard G PestellDepartment of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, 19107, USA.
Kongming WuDepartment of Oncology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. kmwu@tjh.tjmu.edu.cn.ORCID 0000-0003-2499-1032
Tongji Hospital · CNThomas Jefferson University · US

Funding

DACH1/Eya Cell fate determination factor and mammary tumorigenesisR01CA132115 · NCI · THOMAS JEFFERSON UNIVERSITY · PI PESTELL, RICHARD G · 2009 to 2018
$3.1M
NCI NIH HHS R01 CA132115
6 · The paper itself

Abstract

Dachshund homolog 1 (DACH1), a key cell fate determination factor, contributes to tumorigenesis, invasion, metastasis of human breast neoplasm. However, the exact molecular mechanisms for the anti-tumor roles of DACH1 in breast carcinoma are still lack of extensive understanding. Herein, we utilized immunohistochemistry (IHC) staining and public microarray data analysis showing that DACH1 was higher in normal breast, low-grade and luminal-type cancer in comparison with breast carcinoma, high-grade and basal-like tumors respectively. Additionally, both correlation analysis of public databases of human breast carcinoma and IHC analysis of mice xenograft tumors demonstrated that DACH1 inversely related to cancer stem cells (CSCs) markers, epithelial-mesenchymal transition (EMT) inducers and basal-enriched molecules, while cluster of differentiation 44 (CD44) behaved in an opposite manner. Furthermore, mice transplanted tumor model indicated that breast cancer cells Met-1 with up-regulation of DACH1 were endowed with remarkably reduced potential of tumorigenesis. Importantly, meta-analysis of 19 Gene Expression Omnibus (GEO) databases of breast cancer implicated that patients with higher DACH1 expression had prolonged time to death, recurrence and metastasis, while CD44 was a promising biomarker predicting worse overall survival (OS) and metastasis-free survival (MFS). Collectively, our study indicated that CD44 might be a novel target of DACH1 in breast carcinoma.

Indexed as

BiomarkersBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticEpithelial-Mesenchymal TransitionErbB ReceptorsEye ProteinsFemaleFibronectinsGene Expression Regulation, NeoplasticGranzymesHumansHyaluronan ReceptorsImmunohistochemistryKi-67 AntigenNeoplasm GradingBiomarkersCD44 protein, humanDACH1 protein, humanEGFR protein, humanErbB ReceptorsEye ProteinsFibronectinsGranzymesGZMM protein, humanHyaluronan ReceptorsKi-67 AntigenProto-Oncogene Proteins c-mycSOX2 protein, humanSOXB1 Transcription FactorsTranscription FactorsVimentin

Identifiers

PMID28659634
PMCPMC5489534
OpenAlexW2702927692

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.