Evidence map›Paper›PMID 30654191›Full record

ArticleMolecular therapy. Nucleic acids2019

The Modulatory Role of MicroRNA-873 in the Progression of KRAS-Driven Cancers.

Hamada A Mokhlis, Recep Bayraktar, Nashwa N Kabil, Ayse Caner, Nermin Kahraman, Cristian Rodriguez-Aguayo, Erika P Zambalde, Jianting Sheng, Kübra Karagoz, Pinar Kanlikilicer and 8 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  9. Involvement of FAM170B-AS1, hsa-miR-1202, and hsa-miR-146a-5p in breast cancer.Cancer biomarkers : section A of Disease markers · 2024
    Article
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  17. Non-coding RNAs and potential therapeutic targeting in cancer.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  18. Review
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  20. An engineered chimeric toxin that cleaves activated mutant and wild-type RAS inhibits tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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

18 authors at 5 institutions in 2 countries.

Hamada A MokhlisDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Department of Pharmacology and Toxicology, Faculty of Pharmacy, The University of Al-Azhar, Cairo, Egypt.
Recep BayraktarDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Nashwa N KabilDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ayse CanerDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Nermin KahramanDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Cristian Rodriguez-AguayoDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Erika P ZambaldeDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Jianting ShengDepartment of Systems Medicine & Bioengineering, Houston Methodist Institute for Academic Medicine Research Institute, Houston Methodist Weill Cornell Medical College, Houston, TX, USA.
Kübra KaragozRutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Pinar KanlikilicerDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Abdel Aziz H Abdel AzizDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, The University of Al-Azhar, Cairo, Egypt.
Tamer M AbdelghanyDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, The University of Al-Azhar, Cairo, Egypt.
Ahmed A AshourDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, The University of Al-Azhar, Cairo, Egypt.
Stephen WongDepartment of Systems Medicine & Bioengineering, Houston Methodist Institute for Academic Medicine Research Institute, Houston Methodist Weill Cornell Medical College, Houston, TX, USA.
Michael L GatzaRutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
George A CalinDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Center for RNA Interference and Non-Coding RNAs, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Gabriel Lopez-BeresteinDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Center for RNA Interference and Non-Coding RNAs, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Bulent OzpolatDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA; Center for RNA Interference and Non-Coding RNAs, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: bozpolat@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USAl-Azhar University · EGRutgers, The State University of New Jersey · USHouston Methodist · USMethodist Hospital · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Functional Proteomics by Reverse Phase Protein Array in CancerR50CA221675 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LU, YILING · 2017 to 2021
$726k
NCI NIH HHS P30 CA016672NCI NIH HHS R50 CA221675
6 · The paper itself

Abstract

KRAS is one of the most frequently mutated proto-oncogenes in pancreatic ductal adenocarcinoma (PDAC) and aberrantly activated in triple-negative breast cancer (TNBC). A profound role of microRNAs (miRNAs) in the pathogenesis of human cancer is being uncovered, including in cancer therapy. Using in silico prediction algorithms, we identified miR-873 as a potential regulator of KRAS, and we investigated its role in PDAC and TNBC. We found that reduced miR-873 expression is associated with shorter patient survival in both cancers. miR-873 expression is significantly repressed in PDAC and TNBC cell lines and inversely correlated with KRAS levels. We demonstrate that miR-873 directly bound to the 3' UTR of KRAS mRNA and suppressed its expression. Notably, restoring miR-873 expression induced apoptosis; recapitulated the effects of KRAS inhibition on cell proliferation, colony formation, and invasion; and suppressed the activity of ERK and PI3K/AKT, while overexpression of KRAS rescued the effects mediated by miR-873. Moreover, in vivo delivery of miR-873 nanoparticles inhibited KRAS expression and tumor growth in PDAC and TNBC tumor models. In conclusion, we provide the first evidence that miR-873 acts as a tumor suppressor by targeting KRAS and that miR-873-based gene therapy may be a therapeutic strategy in PDAC and TNBC.

Indexed as

breast cancergene regulationgene silencinginvasionKRASliposomesmicroRNAmiR-873nanoparticlesncRNAnon-coding RNAoncogenepancreatic cancerproliferationtherapytriple-negative breast cancertumorigenesis

Identifiers

PMID30654191
PMCPMC6348737
OpenAlexW2905038838

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.