Evidence map›Paper›PMID 21970405›Full record

ArticleBMC cancer2011

MiR-125b promotes proliferation and migration of type II endometrial carcinoma cells through targeting TP53INP1 tumor suppressor in vitro and in vivo.

Feizhou Jiang, Te Liu, Yinyan He, Qin Yan, Xiaoyue Chen, Hui Wang, Xiaoping Wan

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
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  5. The Role of Microbiota in the Immunopathogenesis of Endometrial Cancer.International journal of molecular sciences · 2022
    Review
  6. miR 31-3p Has the Highest Expression in Cesarean Scar Endometriosis.International journal of molecular sciences · 2022
    Article
  7. Article
  8. MicroRNA-641 Inhibits Endometrial Cancer Progression via Targeting AP1G1.Evidence-based complementary and alternative medicine : eCAM · 2022
    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

7 authors at 2 institutions in 1 country.

Feizhou JiangDepartment of Obstetrics and Gynecology, Shanghai Jiaotong University Affiliated International Peace Maternity & Child Health Hospital of the China Welfare Institute, Shanghai, China.
Te Liu
Yinyan He
Qin Yan
Xiaoyue Chen
Hui Wang
Xiaoping Wan
International Peace Maternity & Child Health Hospital · CNShanghai First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur previous studies have identified that miR-125b was overexpressed in type II endometrial carcinoma (EC) cells compared with type I using microRNAs microarray. Although recent studies have shown the important role of miR-125b in several tumors and overexpression of miR-125b in advanced EC, its function in this disease has not yet been defined. In the present study, we tried to confirm the result of microRNAs microarray and further investigated the functions of miR-125b in EC, and tried to find new downstream targets of miR-125b.

methodsDifferential expression of miR-125b was detected between type II EC cells (KLE, AN3CA) with ER negative and type I EC cells (ishikawa, RL95-2) with ER positive by qRT-PCR and northern blotting. The effects of miR-125b of on proliferation, migration, and target protein expression were evaluated by CCK8 assay, wound healing assay, transwell migration assay, western blotting, and Tumorigenicity assays in nude mice. In addition, luciferase reporter plasmid was constructed to demonstrate the direct target of miR-125b.

resultsMiR-125b was overexpressed in type II EC cells compared with type I. Exogenous miR-125b expression increased proliferation and migration of ishikawa cells and abrogating expression of miR-125b suppressed proliferation, and migration of AN3CA cells in vitro. In addition, in vivo tumor formation assay confirmed that forced miR-125b expression promoted proliferation potential of ishikawa cells, and tumor suppressor gene Tumor Protein 53-Induced Nuclear Protein 1 (TP53INP1) was identified to be the direct target of miR-125b.

conclusionsTP53INP1 was newly identified to be the direct downstream target of miR-125b. MiR-125b, which was overexpressed in type II EC cells compared with type I, contributes to malignancy of type II EC possibly through down-regulating TP53INP1.

Indexed as

AnimalsCarrier ProteinsCell MovementCell ProliferationEndometrial NeoplasmsFemaleGene Expression Regulation, NeoplasticHeat-Shock ProteinsHumansMiceMice, NudeMicroRNAsTumor BurdenTumor Suppressor ProteinsXenograft Model Antitumor AssaysCarrier ProteinsHeat-Shock ProteinsMicroRNAsMIRN125 microRNA, humanTP53INP1 protein, humanTumor Suppressor Proteins

Identifiers

PMID21970405
PMCPMC3210504
OpenAlexW2162289930

What OpenQuestion holds

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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.