Evidence map›Paper›PMID 29556333›Full record

ArticleJournal of Cancer2018

Upregulation of HES1 Promotes Cell Proliferation and Invasion in Breast Cancer as a Prognosis Marker and Therapy Target via the AKT Pathway and EMT Process.

Xiaoying Li, Yu Cao, Mu Li, Feng Jin

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Molecular docking andToxicology reports · 2024
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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

4 authors at 2 institutions in 1 country.

Xiaoying LiDepartment of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Yu CaoDepartment of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Mu LiDepartment of General Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Feng JinDepartment of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HES1 is a transcriptional repressor involved in cell differentiation and proliferation as well as in various cancer developments, but its expression pattern and biological roles in breast cancer have not been examined. In this study, we assessed HES1 expression in breast cancer tissues using immunohistochemistry and Western blot analyses and investigated HES1 function using MTT and Matrigel invasion assays. Significant relationships were observed between HES1 upregulation and advanced TNM stage (p=0.011), node metastasis (p=0.043), negative oestrogen receptor expression (p=0.001) and triple-negative status (p=0.001). HES1 overexpression was correlated with poor prognosis in breast cancer patients (p<0.05). The MTT and Matrigel invasion assays showed that silencing HES1 in MDA-MB-231 cells decreased cell proliferation and invasion, whereas overexpression of HES1 in MCF-7 cells enhanced its proliferation and invasion. Further analyses showed that silencing HES1 downregulated p-AKT and impeded epithelial-mesenchymal transition (EMT), whereas overexpression of HES1 upregulated AKT phosphorylation and induced EMT. Our study demonstrated that HES1 upregulation is a predictor of poor prognosis in human breast cancers and might be a critical contributor to the proliferation and invasion of breast cancer cells. Moreover, the proportion of cells with overexpression of HES1 in triple-negative breast cancer (TNBC) samples was significantly higher. Thus, HES1 might be a potential therapeutic target in the treatment of TNBC.

Indexed as

AKTepithelial-mesenchymal transition (EMT)HES1phosphatase and tensin homologue (PTEN)prognosistriple-negative breast cancer (TNBC)

Identifiers

PMID29556333
PMCPMC5858497
OpenAlexW2792949176

What OpenQuestion holds

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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.