Evidence map›Paper›PMID 33173276›Full record

ArticleDrug design, development and therapy2020

Pristimerin Suppresses Trophoblast Cell Epithelial-Mesenchymal Transition via miR-542-5p/EGFR Axis.

Chang Shu, Xiaowei Yu, Shihuan Cheng, Jili Jing, Cong Hu, Bo Pang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Coenzyme Q10 Stimulate Reproductive Vatality.Drug design, development and therapy · 2023
    Review
  6. MicroRNA Dysregulation in Prostate Cancer.Pharmacogenomics and personalized medicine · 2022
    Article
  7. Article
  8. 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

6 authors at 1 institution in 1 country.

Chang Shu *Department of Obstetrics and Gynecology, The First Hospital of Jilin University, Changchun, Jilin 130021, People's Republic of China.
Xiaowei Yu *Centre for Reproductive Medicine, Centre for Prenatal Diagnosis, The First Hospital of Jilin University, Changchun, Jilin 130021, People's Republic of China.
Shihuan ChengDepartment of Rehabilitation, The First Hospital of Jilin University, Changchun, Jilin 130021, People's Republic of China.ORCID 0000-0001-7661-1543
Jili JingCentre for Reproductive Medicine, Centre for Prenatal Diagnosis, The First Hospital of Jilin University, Changchun, Jilin 130021, People's Republic of China.
Cong HuCentre for Reproductive Medicine, Centre for Prenatal Diagnosis, The First Hospital of Jilin University, Changchun, Jilin 130021, People's Republic of China.ORCID 0000-0002-8595-4713
Bo PangCentral Laboratory, The First Hospital of Jilin University, Changchun, Jilin 130021, People's Republic of China.ORCID 0000-0003-1667-4846
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEctopic pregnancy (EP) is an ectopic embryo implantation occurred outside the uterine cavity. Nowadays, more attention have garnered in fast and effective treatment with less side effects. Pristimerin is known as the clinical application for anti-cancer, and the effect on EP therapy is still unclear. MATERIALS AND

methodsTrophoblast cell line HTR-8/SVneo was used; then, we performed cell counting kit-8 assay, wound healing assay, flow cytometry and real-time polymerase chain reaction analysis (RT-PCR) to detect the cell viability, migration ability, apoptosis and epithelial-mesenchymal transition (EMT) under pristimerin treatment. In addition, public bioinformatic database was used to discover the connection between molecular and genes. Finally, we used miRNA transfection and RT-PCR techniques to determine the underlying molecular mechanism.

resultsWe revealed that pristimerin inhibited trophoblast cells proliferation, migration and EMT, while induced trophoblast cell apoptosis. Furthermore, expression of miR-542-5p, AGO2 and EGFR was suppressed in HTR-8/SVneo cells post pristimerin treatment, and miR-542-5p silence showed the same effect. Combing pristimerin treatment and miR-542-5p silence showed a synergistic action.

conclusionPristimerin could be an effective treatment to block embryo implantation by miR-542-5p and EGFR down-regulation.

Indexed as

AnimalsApoptosisCell MovementCell ProliferationCells, CulturedDose-Response Relationship, DrugEpithelial-Mesenchymal TransitionErbB ReceptorsFemaleInjections, IntraperitonealMiceMice, Inbred C57BLMicroRNAsMolecular StructurePentacyclic TriterpenesSignal Transductioncelastrol methyl esterEGFR protein, mouseErbB ReceptorsMicroRNAsMIRN542 microRNA, mousePentacyclic TriterpenesEGFRmiR-542-5ppristimerintrophoblast cellunruptured ectopic pregnancy

Identifiers

PMID33173276
PMCPMC7646443
OpenAlexW3097884505

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.