Evidence map›Paper›PMID 30584335›Full record

ArticleOncoTargets and therapy2018

miR-1 inhibits the proliferation of breast cancer stem cells by targeting EVI-1.

Lei Wu, Tianyi Wang, Dongning He, Xiaoxi Li, Youhong Jiang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The important role of miR-1-3p in cancers.Journal of translational medicine · 2023
    Review
  5. Review
  6. MicroRNA-1: Diverse role of a small player in multiple cancers.Seminars in cell & developmental biology · 2022
    Review
  7. Article
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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

5 authors at 3 institutions in 2 countries.

Lei WuMolecular Oncology Laboratory of Cancer Research Institute, The First Hospital of China Medical University, Shenyang 110001, China, jiangyouhong2000@aliyun.com.
Tianyi WangDepartment of Medical Oncology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121001, China.
Dongning HeDepartment of Medical Oncology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121001, China.
Xiaoxi LiMolecular Oncology Laboratory of Cancer Research Institute, The First Hospital of China Medical University, Shenyang 110001, China, jiangyouhong2000@aliyun.com.
Youhong JiangMolecular Oncology Laboratory of Cancer Research Institute, The First Hospital of China Medical University, Shenyang 110001, China, jiangyouhong2000@aliyun.com.
Jinzhou Medical University · CNMolecular Oncology (United States) · USFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeBreast cancer stem cells (BCSCs) have been regarded as the key factor for treatment failure in breast cancer. The abnormal expression of miRNAs plays a significant role in different tumor types. However, the role of miR-1 in breast cancer remains poorly understood. The purpose of this study was to evaluate the effects of miR-1 on the proliferation and apoptosis of BCSCs. MATERIALS AND

methodsCD44

resultsIn this study, we demonstrated that miR-1 was significantly downregulated in breast cancer tissues compared to the adjacent non-tumor tissues. The luciferase reporter assay verified that EVI-1 was a direct target of miR-1, and upregulation of miR-1 negatively correlated with the expression of EVI-1 in BCSCs at both the transcriptional and posttranslational levels. Furthermore, overexpression of miR-1 inhibited BCSCs proliferation and promoted apoptosis, which was reversed by the overexpression of EVI-1. In addition, we demonstrated that aberrant expression of miR-1 could regulate EMT-related genes in BCSCs. Finally, immunohistochemical staining demonstrated that EVI-1 expression was decreased in BCSCs tumors following intra-tumoral miR-1 agomir treatment compared to the control group.

conclusionmiR-1 can negatively regulate the expression of EVI-1 and, thus, affect BCSCs proliferation, apoptosis, and EMT-related markers. Taken together, these findings demonstrate that miR-1 could be employed as a therapeutic strategy in the treatment of breast cancer.

Indexed as

apoptosisbreast cancerEVI-1miR-1proliferation

Identifiers

PMID30584335
PMCPMC6287527
OpenAlexW2902315999

What OpenQuestion holds

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LicenceCC BY-NC
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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.