Evidence map›Paper›PMID 31874105›Full record

ArticleThe Journal of clinical investigation2020

The Mir181ab1 cluster promotes KRAS-driven oncogenesis and progression in lung and pancreas.

Karmele Valencia, Oihane Erice, Kaja Kostyrko, Simone Hausmann, Elizabeth Guruceaga, Anuradha Tathireddy, Natasha M Flores, Leanne C Sayles, Alex G Lee, Rita Fragoso and 14 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

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  16. Identification of aFrontiers in cellular and infection microbiology · 2022
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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

24 authors at 11 institutions in 3 countries.

Karmele ValenciaUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Oihane EriceUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Kaja KostyrkoDivision of Hematology and Oncology, UCSF, San Francisco, California, USA.
Simone HausmannDepartment of Experimental Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Elizabeth GuruceagaBioinformatics Platform, Center for Applied Medical Research, Pamplona, Spain.
Anuradha TathireddyDepartment of Pediatrics, and.
Natasha M FloresDepartment of Experimental Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Leanne C SaylesDivision of Hematology and Oncology, UCSF, San Francisco, California, USA.
Alex G LeeDivision of Hematology and Oncology, UCSF, San Francisco, California, USA.
Rita FragosoDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Tian-Qiang SunAchelois Oncology, Redwood City, California, USA.
Adrian VallejoUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Marta RomanUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Rodrigo Entrialgo-CadiernoUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Itziar MiguelizUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Nerea RazquinUniversity of Navarra, Center for Applied Medical Research, Program in Gene Therapy and Regulation of Gene Expression, Pamplona, Spain.
Puri FortesUniversity of Navarra, Center for Applied Medical Research, Program in Gene Therapy and Regulation of Gene Expression, Pamplona, Spain.
Fernando LecandaUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Jun LuGenetics Department, Yale University, New Haven, Connecticut, USA.
Mariano Ponz-SarviseUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Chang-Zheng ChenDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Pawel K MazurDepartment of Experimental Radiation Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
E Alejandro Sweet-CorderoDivision of Hematology and Oncology, UCSF, San Francisco, California, USA.
Silvestre VicentUniversity of Navarra, Center for Applied Medical Research, Program in Solid Tumors, Pamplona, Spain.
Universidad de Navarra · ESUniversity of California, San Francisco · USThe University of Texas MD Anderson Cancer Center · USClovis Oncology (United States) · USNavarre Institute of Health Research · ESBC Platforms (Finland) · FICentro de Investigación Biomédica en Red de Cáncer · ESClinica Universidad de Navarra · ESPediatrics and Genetics · USStanford University · USYale University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V., MINNA, JOHN D. · 1996 to 2024
$57.4M
The Role of Pre-miRNA Loop in Target Regulation by microRNA GenesDP1OD006435 · OD · STANFORD UNIVERSITY · PI CHEN, CHANG-ZHENG · 2009 to 2011
$2.4M
MicroRNAs as T cell sensitivity RheostatsR01AI073724 · NIAID · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2009 to 2013
$2.0M
Novel effectors of Kras in oncogenesis, senescence and tumor progressionR01CA129562 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SWEET-CORDERO, ERIC ALEJANDRO · 2009 to 2016
$1.9M
The SMYD3-ERK5 signaling module in pancreatic cancerR00CA197816 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MAZUR, PAWEL K. · 2017 to 2019
$732k
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS R00 CA197816NCI NIH HHS R01 CA129562NIAID NIH HHS R01 AI073724NIH HHS DP1 OD006435Worldwide Cancer Research 16-0224
6 · The paper itself

Abstract

Few therapies are currently available for patients with KRAS-driven cancers, highlighting the need to identify new molecular targets that modulate central downstream effector pathways. Here we found that the microRNA (miRNA) cluster including miR181ab1 is a key modulator of KRAS-driven oncogenesis. Ablation of Mir181ab1 in genetically engineered mouse models of Kras-driven lung and pancreatic cancer was deleterious to tumor initiation and progression. Expression of both resident miRNAs in the Mir181ab1 cluster, miR181a1 and miR181b1, was necessary to rescue the Mir181ab1-loss phenotype, underscoring their nonredundant role. In human cancer cells, depletion of miR181ab1 impaired proliferation and 3D growth, whereas overexpression provided a proliferative advantage. Lastly, we unveiled miR181ab1-regulated genes responsible for this phenotype. These studies identified what we believe to be a previously unknown role for miR181ab1 as a potential therapeutic target in 2 highly aggressive and difficult to treat KRAS-mutated cancers.

Indexed as

Multigene FamilyAnimalsCarcinogenesisCell Line, TumorCell ProliferationHumansLung NeoplasmsMiceMice, KnockoutMicroRNAsNeoplasms, ExperimentalPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)RNA, NeoplasmHras protein, mouseKRAS protein, humanMicroRNAsMIrn181 microRNA, humanmirn181 microRNA, mouseProto-Oncogene Proteins p21(ras)RNA, NeoplasmMouse modelsNoncoding RNAsOncogenesOncology

Identifiers

PMID31874105
PMCPMC7108928
OpenAlexW2997902533

What OpenQuestion holds

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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.