Evidence map›Paper›PMID 31410735›Full record

ArticleBreast cancer (Tokyo, Japan)2020

miR-638 represses the stem cell characteristics of breast cancer cells by targeting E2F2.

Qiu-Yan Lin, Jia-Qi Wang, Li-Li Wu, Wei-E Zheng, Pei-Rui Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

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  8. miR-125b-5p, miR-155-3p, and miR-214-5p and TargetInternational journal of molecular sciences · 2023
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  10. Expression Profiles ofBiomedicines · 2022
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  11. Review
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  16. Review
  17. 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 2 institutions in 1 country.

Qiu-Yan LinDepartment of Medical Oncology, Ruian People's Hospital, Wansong Road No. 108, Wenzhou, 325200, Zhejiang, China.
Jia-Qi WangDepartment of Medical Oncology, Ruian People's Hospital, Wansong Road No. 108, Wenzhou, 325200, Zhejiang, China.
Li-Li WuDepartment of Medical Oncology, Ruian People's Hospital, Wansong Road No. 108, Wenzhou, 325200, Zhejiang, China.
Wei-E ZhengDepartment of Medical Oncology, Ruian People's Hospital, Wansong Road No. 108, Wenzhou, 325200, Zhejiang, China.
Pei-Rui ChenDepartment of Medical Oncology, Ruian People's Hospital, Wansong Road No. 108, Wenzhou, 325200, Zhejiang, China. PeiRuiChenrop@163.com.
Wenzhou Medical University · CNRuian People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe miR-638 acted as a tumor suppressor and E2F transcription factor 2 (E2F2) was a critical regulator in some cancers, while the role of them on stemness of breast cancer stem cells (BCSCs) was rarely detailed. Hence, we focused on exploring the effects of miR-638 and E2F2 on BCSCs stemness.

methodsThe proportion of CD24 -/CD44 + cells of BCSCs was detected by flow cytometry. The target relationship of miR-638 and E2F2 was explored using luciferase assays. The ability of self-renewal, proliferation, and invasion of BCSCs were determined by Mammosphere forming, Cell Counting Kit-8 (CCK-8), colony formation, and transwell assays. Xenograft tumor was established to detect the influence of miR-638 on tumor growth.

resultsmiR-638 was down-regulated, while E2F2 was elevated in breast cancer. The E2F2 level was negatively correlated with miR-638. The BCSCs represented higher proportion of CD24 -/CD44 + cells and levels of sex determining region Y-box 2 (SOX2) and octamer-binding transcription factor 4 (OCT4). The miR-638 was down-regulated and E2F2 was increased in BCSCs. MiR-638 could target to E2F2 and decreased the level of E2F2 in BCSCs cells. Overexpression of miR-638 decreased the proportion of CD24 -/CD44 + cells and the levels of SOX2 and OCT4 by inhibiting E2F2. The overexpression of miR-638 also inhibited the abilities of self-renewal, proliferation, and invasion of BCSCs by inhibiting E2F2. The miR-638 overexpression inhibited the breast tumor growth.

conclusionMiR-638 represses the characteristics and behaviors of BCSCs by targeting E2F2. MiR-638 may be a potential target for breast cancer therapy.

Indexed as

AnimalsBinding SitesBreast NeoplasmsCell ProliferationCell Self RenewalE2F2 Transcription FactorFemaleGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsMCF-7 CellsMiceMice, NudeMicroRNAsNeoplasm TransplantationNeoplastic Stem CellsCD44 protein, humanE2F2 protein, humanE2F2 Transcription FactorHyaluronan ReceptorsMicroRNAsMIRN638 microRNA, humanRNA, Small InterferingBCSCsCCK-8E2F2miR-638Stemness

Identifiers

PMID31410735
OpenAlexW2968153232

What OpenQuestion holds

Textmetadata
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.