Evidence map›Paper›PMID 29471243›Full record

ArticleTranslational oncology2018

TRPS1 Suppresses Breast Cancer Epithelial-mesenchymal Transition Program as a Negative Regulator of SUZ12.

Jing Hu, Peng Su, Meng Jiao, Xinnuo Bai, Mei Qi, Hui Liu, Zhen Wu, Jingtian Sun, Gengyin Zhou, Bo Han

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

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  18. Role of p38γ MAPK in regulation of EMT and cancer stem cells.Biochimica et biophysica acta. Molecular basis of disease · 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

10 authors at 2 institutions in 1 country.

Jing HuDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.
Peng SuDepartment of Pathology, Shandong University Qilu Hospital, Jinan, 250012, China.
Meng JiaoDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.
Xinnuo BaiDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.
Mei QiDepartment of Pathology, Shandong University Qilu Hospital, Jinan, 250012, China.
Hui LiuDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.
Zhen WuDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.
Jingtian SunDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China.
Gengyin ZhouDepartment of Pathology, Shandong University Qilu Hospital, Jinan, 250012, China.
Bo HanDepartment of Pathology, Shandong University, School of Basic Medicine, Jinan, 250012, China; Department of Pathology, Shandong University Qilu Hospital, Jinan, 250012, China. Electronic address: boh@sdu.edu.cn.
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) is among the most common malignant diseases and metastasis is the handcuff of treatment. Cancer metastasis is a multistep process associated with the epithelial-mesenchymal transition (EMT) program. Several studies have demonstrated that transcriptional repressor GATA binding 1 (TRPS1) played important roles in development and progression of primary BC. In this study we sought to identify the mechanisms responsible for this function of TRPS1 in the continuum of the metastatic cascade. Here we described that TRPS1 was significantly associated with BC metastasis using public assessable datasets. Clinically, loss of TRPS1 expression in BC was related to higher histological grade. In vitro functional study and bioinformatics analysis revealed that TRPS1 inhibited cell migration and EMT in BC. Importantly, we identified SUZ12 as a novel target of TRPS1 related to EMT program. ChIP assay demonstrated TRPS1 directly inhibited SUZ12 transcription by binding to the SUZ12 promoter. Loss of TRPS1 resulted in increased SUZ12 binding and H3K27 tri-methylation at the CDH1 promoter and repression of E-cadherin. In all, our data indicated that TRPS1 maintained the expression of E-cadherin by inhibiting SUZ12, which might provide novel insight into how loss of TRPS1 contributed to BC progression.

Identifiers

PMID29471243
PMCPMC5884189
OpenAlexW2790730492

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.