Evidence map›Paper›PMID 34313525›Full record

ArticleCell cycle (Georgetown, Tex.)2021

Piwi-interacting RNA-651 promotes cell proliferation and migration and inhibits apoptosis in breast cancer by facilitating DNMT1-mediated PTEN promoter methylation.

Ting Liu, Juan Wang, Lei Sun, Miao Li, Xin He, Jue Jiang, Qi Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
8.2field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Ting LiuDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Juan WangDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Lei SunDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Miao LiDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Xin HeDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Jue JiangDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Qi ZhouDepartment of Ultrasound, The Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China.
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Piwi-interacting RNAs (piRNAs/piRs) are small non-coding RNAs that play important roles in stablizing genome through silencing transposable genetic elements. The piR-651 was reported to be dysregulated in several human solid cancer tissues, such as gastric and lung cancers. However, the role of piRNA-651 in carcinogenesis of breast cancer has not been defined. We found that piR-651 was highly expressed in breast cancer tissues and cell lines. Overexpression of piR-651 facilitated cell proliferation and invasion, restrained cell apoptosis and the percentage of arrested cells in G0/G1 phase, accompanied by upregulated expression of oncogenes (MDM2, CDK4 and Cyclin D1), whereas piR-651 downregulation showed the opposite effects. Additionally, piR-651 could promote phosphatase and tensin homolog (PTEN) methylation and its downregulated expression by recruiting DNA methyltransferase 1 (DNMT1) to the PTEN promoter region through complex formation with PIWIL2. PTEN overexpression reversed the effects of upregulated piR-651 on cell functions. This study reveals that piR-651 promotes proliferation and migration and induces apoptosis of breast cancer cells by facilitating DNMT1-mediated PTEN promoter methylation, which may provide a potential therapeutic mechanism for breast cancer.

Indexed as

ApoptosisCell MovementCell ProliferationDNA MethylationEpigenesis, GeneticAdultBreast NeoplasmsCell Line, TumorDNA (Cytosine-5-)-Methyltransferase 1FemaleGene Expression Regulation, NeoplasticHumansMiddle AgedNeoplasm InvasivenessPromoter Regions, GeneticPTEN PhosphohydrolaseDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanPTEN PhosphohydrolasePTEN protein, humanRNA, Small InterferingBreast cancerDNMT1methylationpiR-651PTEN

Identifiers

PMID34313525
PMCPMC8409782
OpenAlexW3185150126

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.