Evidence map›Paper›PMID 32983239›Full record

ArticleCellular & molecular biology letters2020

Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1.

Minhao Lv, Qixin Mao, Juntao Li, Jianghua Qiao, Xiuchun Chen, Suxia Luo

Open access · goldAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Expression and Significance of LINC02418 in Breast Cancer.Breast cancer (Dove Medical Press) · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. The Emerging Roles of LINC00665 in Human Cancers.Frontiers in cell and developmental biology · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Article
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

6 authors at 1 institution in 1 country.

Minhao LvDepartment of Breast Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan P.R. China.
Qixin MaoDepartment of Breast Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan P.R. China.
Juntao LiDepartment of Breast Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan P.R. China.
Jianghua QiaoDepartment of Breast Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan P.R. China.
Xiuchun ChenDepartment of Breast Surgery, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan P.R. China.
Suxia LuoDepartment of Medical Oncology, The Affiliated Cancer Hospital of Zhengzhou University, No. 127, Dongming Road, Jinshui District, Zhengzhou, 450008 Henan P.R. China.ORCID 0000-0001-6805-7650
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown.

methodsLINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis.

resultsLINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p.

conclusionLINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.

Indexed as

Apoptosisbeta CateninBinding, CompetitiveBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsRNA, Long NoncodingUp-Regulationbeta CateninCTNNB1 protein, humanMicroRNAsMIRN-3619 microRNA, humanRNA, Long NoncodingBreast cancerCTNNB1LINC00665miR-3619-5pβ-Catenin

Identifiers

PMID32983239
PMCPMC7513511
OpenAlexW3088659359

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.