Evidence map›Paper›PMID 28620240›Full record

ArticleScientific reports2017

miR-200c-driven Mesenchymal-To-Epithelial Transition is a Therapeutic Target in Uterine Carcinosarcomas.

Jill H Tseng, Maria Bisogna, Lien N Hoang, Narciso Olvera, Cristian Rodriguez-Aguayo, Gabriel Lopez-Berestein, Anil K Sood, Douglas A Levine, Petar Jelinic

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  4. Uterine carcinosarcoma: Unraveling the role of epithelial-to-mesenchymal transition in progression and therapeutic potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

9 authors at 3 institutions in 1 country.

Jill H TsengGynecology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
Maria BisognaGynecology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
Lien N HoangDepartment of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.
Narciso OlveraGynecologic Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Langone Medical Center, New York, NY, 10016, USA.
Cristian Rodriguez-AguayoDepartment of Experimental Therapeutics, Houston, TX, 77030, USA.ORCID 0000-0002-7880-7723
Gabriel Lopez-BeresteinDepartment of Experimental Therapeutics, Houston, TX, 77030, USA.
Anil K SoodCenter for RNA Interference and Non-Coding RNA, Houston, TX, 77030, USA.
Douglas A LevineGynecologic Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Langone Medical Center, New York, NY, 10016, USA.ORCID 0000-0003-1038-8232
Petar JelinicGynecologic Oncology, Laura and Isaac Perlmutter Cancer Center, NYU Langone Medical Center, New York, NY, 10016, USA. petar.jelinic@nyumc.org.ORCID 0000-0002-7361-5239
Gynecologic Oncology Group · USMemorial Sloan Kettering Cancer Center · USIo Therapeutics (United States) · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

Uterine carcinosarcomas (UCSs) are highly aggressive malignancies associated with poor prognoses and limited treatment options. These tumors are hypothesized to develop from the endometrial adenocarcinoma (EAC) through epithelial-mesenchymal transition (EMT). We test this long-standing hypothesis by depleting miR-200, a family of microRNAs critical for EMT, in EAC cell lines. Our data suggest that UCSs do not develop from EACs via EMT. Clinically more relevant, we show that miR-200 expression in UCS cells induces a robust mesenchymal-epithelial transition (MET). Using in vitro and murine xenograft models, we demonstrate decreased growth and aggressiveness of miR-200-overexpressing UCS cell lines. Whole transcriptome analysis confirmed changes consistent with an MET and also revealed changes in angiogenic genes expression. Finally, by treatment of UCS-xenografted mice with miR-200c incorporated in DOPC nanoliposomes, we demonstrate anti-tumor activities. These findings suggest that ectopic miR-200 expression using advanced microRNA therapeutics may be a potential treatment approach for patients with UCS.

Indexed as

AnimalsCarcinosarcomaCell AdhesionCell MovementCell ProliferationCell SurvivalComputational BiologyDisease Models, AnimalEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiceMicroRNAsMutationMicroRNAsMIRN200 microRNA, human

Identifiers

PMID28620240
PMCPMC5472620
OpenAlexW2622351493

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.