Evidence map›Paper›PMID 32009798›Full record

ArticleOncoTargets and therapy2019

EZH2 Contributes To Cisplatin Resistance In Breast Cancer By Epigenetically Suppressing miR-381 Expression.

Dongwei Dou, Xin Ge, Xinxing Wang, Xiaodong Xu, Zhe Zhang, Jingjing Seng, Zhang Cao, Yuanting Gu, Mingli Han

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

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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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  12. CDC7 as a novel biomarker and druggable target in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
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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

9 authors at 1 institution in 1 country.

Dongwei Dou *Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Xin Ge *Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Xinxing WangDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Xiaodong XuDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Zhe ZhangDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Jingjing SengDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Zhang CaoDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Yuanting GuDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Mingli HanDepartment of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence reveals the vital role of enhancer of zeste homolog 2 (EZH2) in cancer chemoresistance. However, its function and molecular mechanisms in breast cancer chemoresistance remain largely unknown.

methodsGene expression was evaluated using quantitative real-time PCR (qRT-PCR) and Western blot analysis. The functional roles of EZH2 and miR-381 in breast cancer were explored using cell MTT assay and flow cytometry analysis. The effect of EZH2 on miR-381 expression in transcriptional level was determined using Chromatin immunoprecipitation (ChIP) assay and Luciferase reporter assay.

resultsIn this study, we found that EZH2 was up-regulated in CDDP-resistant breast cancer tissues and cell lines. Breast cancer patients with high EZH2 expression had a poor prognosis. EZH2 silencing improved the sensitivity of MCF-7/CDDP and MDA-MB-231/CDDP cells towards CDDP. Moreover, EZH2 could epigenetically silence miR-381. miR-381 overexpression could overcome CDDP resistance in CDDP-resistant breast cancer cells. miR-381 knockdown weakened the inductive effect of EZH2 silencing on CDDP sensitivity of MCF-7/CDDP and MDA-MB-231/CDDP cells. Furthermore, EZH2 knockdown facilitated CDDP sensitivity of CDDP-resistant breast cancer cells in vivo.

conclusionsCollectively, EZH2 depletion overcame CDDP resistance of breast cancer through epigenetically silencing miR-381, providing a novel therapeutic target for breast cancer chemoresistance.

Indexed as

breast cancerCDDPenhancer of zeste homolog 2miR-381

Identifiers

PMID32009798
PMCPMC6859472
OpenAlexW2983467577

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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.