Evidence map›Paper›PMID 28743276›Full record

ArticleJournal of ovarian research2017

Suppressing miR-199a-3p by promoter methylation contributes to tumor aggressiveness and cisplatin resistance of ovarian cancer through promoting DDR1 expression.

Yuao Deng, Fang Zhao, Liu Hui, Xiuyun Li, Danyu Zhang, Wang Lin, Zhiqiang Chen, Yingxia Ning

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 83 citations in OpenAlex.

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  15. Clinicopathologic and molecular analysis of aCold Spring Harbor molecular case studies · 2022
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  16. MicroRNAs in Genetic Etiology of Human Diseases.Methods in molecular biology (Clifton, N.J.) · 2022
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  17. MiRNA-221-5p suppressed the Th17/Treg ratio in asthma via RORγt/Foxp3 by targeting SOCS1.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021
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  20. Complex roles of discoidin domain receptor tyrosine kinases in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Review
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

8 authors at 3 institutions in 1 country.

Yuao DengDepartment of Gynecology and Obstetrics, Shenzhen People's Hospital, Shenzhen, 518020, China.
Fang ZhaoDepartment of Infectious Disease, The third people's Hospital of Shenzhen, Shenzhen, 518112, China.
Liu HuiDepartment of Gynecology and Obstetrics, The Twelfth People's Hospital of Guangzho, Guangzhou, 510120, China.
Xiuyun LiDepartment of Gynecology and Obstetrics, Shenzhen People's Hospital, Shenzhen, 518020, China.
Danyu ZhangDepartment of Gynecology and Obstetrics, Shenzhen People's Hospital, Shenzhen, 518020, China.
Wang LinDepartment of Gynecology and Obstetrics, Shenzhen People's Hospital, Shenzhen, 518020, China.
Zhiqiang ChenDepartment of Pathology, Shenzhen People's Hospital, Shenzhen, 518020, China.
Yingxia NingDepartment of Gynecology and Obstetrics, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China. ningyingxia@163.com.
ShenZhen People’s Hospital · CNFirst Affiliated Hospital of Guangzhou Medical University · CNShenzhen Third People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiscoidin Domain Receptor 1 (DDR1) belongs to the family of collagen receptor tyrosine kinases that confers the progression of various cancers. Aberrant expression of DDR1 was detected in several human cancers including ovarian cancer, which had been shown to increase the migration and invasion of tumor cells. However, the precise mechanisms underlying the abnormal expression of DDR1 in ovarian cancer has not been well investigated in previous studies.

resultsIn this work, a negative correlation between DDR1 and a tumor suppressor miRNA, miR-199a-3p, was observed in ovarian cancer tissues. Furthermore, in vitro experimental results confirmed that miR-199a-3p decreased the expression of DDR1 via targeting the 3'UTR of DDR1 mRNA. To explore the mechanisms for miR-199a-3p silence in ovarian cancer, the methylation status of the miR-199a promoter was analyzed in ovarian epithelial or cancer cells by methylation-specific PCR and bisulphite sequencing. As expected, the miR-199a promoter was hypermethylated in ovarian cancer cells but not in normal ovarianepithelial cells. Interestingly, knockdown of DNA methyltransferase 3A (DNMT3A) notably increased miR-199a-3p level and then attenuated the expression of DDR1 in ovarian cancer cells, which suggested that DNMT3A was responsible for the miR-199a promoter hypermethylation. Phenotype experiments showed that overexpression of miR-199a-3p significantly impaired the migratory, invasive, and tumorigenic capabilities of ovarian cancer cells as well as enhanced cisplatin resistance through inhibiting DDR1 expression.

conclusionThese findings demonstrate a critical role of miR-199a-3p/DDR1 pathway in ovarian cancer development.

Indexed as

Ovarian NeoplasmsAgedAntineoplastic AgentsCell LineCell Line, TumorCell MovementCell SurvivalCisplatinDiscoidin Domain Receptor 1DNA MethylationDNA Methyltransferase 3ADrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsAntineoplastic AgentsCisplatinDDR1 protein, humanDiscoidin Domain Receptor 1DNA Methyltransferase 3ADNMT3A protein, humanMicroRNAsmirn199 microRNA, humanCisplatinDiscoidin domain receptor 1 (DDR1)miR-199a-3pOvarian cancer

Identifiers

PMID28743276
PMCPMC5526233
OpenAlexW2737969333

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.