Evidence map›Paper›PMID 26675258›Full record

ArticleOncotarget2016

miR-30a inhibits endothelin A receptor and chemoresistance in ovarian carcinoma.

Rosanna Sestito, Roberta Cianfrocca, Laura Rosanò, Piera Tocci, Elisa Semprucci, Valeriana Di Castro, Valentina Caprara, Gabriella Ferrandina, Andrea Sacconi, Giovanni Blandino and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Endothelin and the tumor microenvironment: a finger in every pie.Clinical science (London, England : 1979) · 2024
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  15. MiR-30a suppresses metastasis of gastric adenocarcinoma via targeting FAPα.Cancer biomarkers : section A of Disease markers · 2020
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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

11 authors at 1 institution in 1 country.

Rosanna SestitoTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Roberta CianfroccaTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Laura RosanòTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Piera TocciTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Elisa SemprucciTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Valeriana Di CastroTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Valentina CapraraTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Gabriella FerrandinaGynecologic Oncology Unit, Catholic University of Rome, Rome, Italy.
Andrea SacconiTranslational Oncogenomic Unit, Regina Elena National Cancer Institute, Rome, Italy.
Giovanni BlandinoTranslational Oncogenomic Unit, Regina Elena National Cancer Institute, Rome, Italy.
Anna BagnatoTranslational Research Functional Departmental Area, Regina Elena National Cancer Institute, Rome, Italy.
Università Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance remains the major clinical barrier to successful treatment in epithelial ovarian carcinoma (EOC) patients, and the evidence of microRNA involvement in drug resistance has been recently emerging. Endothelin-1 (ET-1)/ETA receptor (ETAR) axis is aberrantly activated in chemoresistant EOC cells and elicits pleiotropic effects promoting epithelial-to-mesenchymal transition (EMT) and the acquisition of chemoresistance. However, the relationship between ETAR and miRNA is still unknown. Hence, in this study we evaluated whether dysregulation of miRNA might enhance ETAR expression in sensitive and resistant EOC cells. Based on bioinformatic tools, we selected putative miRNA able to recognize the 3'UTR of ETAR. An inverse correlation was observed between the expression levels of miR-30a and ETAR in both EOC cell lines and tumor samples. miR-30a was found to specifically bind to the 3'UTR of ETAR mRNA, indicating that ETAR is a direct target of miR-30a. Overexpression of miR-30a decreased Akt and mitogen activated protein kinase signaling pathway activation, cell proliferation, invasion, plasticity, EMT marker levels, and vascular endothelial growth factor release. Interestingly, ectopic expression of miR-30a re-sensitized platinum-resistant EOC cells to cisplatinum-induced apoptosis. Consistently, resistant EOC xenografts overexpressing miR-30a resulted in significantly less tumor growth than controls. Together our study provides a new perspective on the regulatory mechanism of ETAR gene. Interestingly, our findings highlight that blockade of ETAR regulatory axis is the mechanism underlying the tumor suppressor function of miR-30a in chemoresistant EOC cells.

Indexed as

AnimalsApoptosisBlotting, WesternCell MovementCell ProliferationDrug Resistance, NeoplasmEnzyme-Linked Immunosorbent AssayFemaleHumansImmunoenzyme TechniquesMiceMice, NudeMicroRNAsOvarian NeoplasmsReal-Time Polymerase Chain ReactionReceptor, Endothelin AMicroRNAsMIRN30b microRNA, humanReceptor, Endothelin ARNA, Messengerchemoresistanceendothelin-1endothelin A receptormiR-30aovarian carcinoma

Identifiers

PMID26675258
PMCPMC4826186
OpenAlexW2285667067

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.