Evidence map›Paper›PMID 31673240›Full record

ArticleInternational journal of medical sciences2019

MicroRNA-425-5p Expression Affects BRAF/RAS/MAPK Pathways In Colorectal Cancers.

Andrea Angius, Giovanna Pira, Antonio Mario Scanu, Paolo Uva, Giovanni Sotgiu, Laura Saderi, Alessandra Manca, Caterina Serra, Elena Uleri, Claudia Piu and 9 more

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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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

19 authors at 4 institutions in 1 country.

Andrea AngiusIstituto di Ricerca Genetica e Biomedica (IRGB), CNR, Cittadella Universitaria di Cagliari, 09042 Monserrato (CA), Italy.
Giovanna PiraDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Antonio Mario ScanuDepartment of Medical, Surgical and Experimental Sciences, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.
Paolo UvaCRS4, Science and Technology Park Polaris, Piscina Manna, 09010 Pula, CA, Italy.
Giovanni SotgiuDepartment of Medical, Surgical and Experimental Sciences, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.
Laura SaderiDepartment of Medical, Surgical and Experimental Sciences, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.
Alessandra MancaDepartment of Pathology, AOU Sassari, Via Matteotti 60, 07100 Sassari, Italy.
Caterina SerraDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Elena UleriDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Claudia PiuDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Maurizio CaocciDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Gabriele IbbaDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Angelo ZinelluDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Maria Rosaria CesaraccioDepartment of Prevention, Registro Tumori Provincia di Sassari, ASSL Sassari-ATS Sardegna, Via Rizzeddu 21, Sassari, Italy.
Francesca SangesDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Maria Rosaria MuroniDepartment of Medical, Surgical and Experimental Sciences, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.
Antonina DoleiDepartment of Biomedical Sciences, University of Sassari, Viale San Pietro 43-b, 07100 Sassari, Italy.
Paolo Cossu-RoccaDepartment of Medical, Surgical and Experimental Sciences, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.
Maria Rosaria De MiglioDepartment of Medical, Surgical and Experimental Sciences, University of Sassari, Viale San Pietro 8, 07100 Sassari, Italy.
University of Sassari · ITAzienda Ospedaliero Universitaria di Sassari · ITEnvironment Park · ITInstitute of Genetic and Biomedical Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is a leading cause of cancer death worldwide and about 20% is metastatic at diagnosis and untreatable. The anti-EGFR therapy in metastatic patients is led by the presence of KRAS-mutations in tumor tissue. KRAS-wild-type CRC patients showed a positive response rate of about 70% to cetuximab or panitumumab combined with chemotherapy. MiRNAs are promising markers in oncology and could improve our knowledge on pathogenesis and drug resistance in CRC patients. This class of molecules represents an opportunity for the development of miRNA-based strategies to overcome the ineffectiveness of anti-EGFR therapy. We performed an integrative analysis of miRNA expression profile between KRAS-mutated CRC and KRAS-wildtype CRC and paired normal colic tissue (NCT). We revealed an overexpression of miR-425-5p in KRAS-mutated CRC compared to KRAS-wild type CRC and NCT and demonstrated that miR-425-5p exerts regulatory effects on target genes involved in cellular proliferation, migration, invasion, apoptosis molecular networks. These epigenetic mechanisms could be responsible of the strong aggressiveness of KRAS-mutated CRC compared to KRAS-wildtype CRC. We proved that some miR-425-5p targeted genes are involved in EGFR tyrosine kinase inhibitor resistance pathway, suggesting that therapies based on miR-425-5p may have strong potential in targeting KRAS-driven CRC. Moreover, we demonstrated a role in the oncogenesis of miR-31-5p, miR-625-5p and miR-579 by comparing CRC versus NCT. Our results underlined that miR-425-5p might act as an oncogene to participate in the pathogenesis of KRAS-mutated CRC and contribute to increase the aggressiveness of this subcategory of CRC, controlling a complex molecular network.

Indexed as

ApoptosisCarcinogenesisCell MovementCell ProliferationCetuximabColorectal NeoplasmsEpigenesis, GeneticErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMutationNeoplasm InvasivenessNeoplasm ProteinsBRAF protein, humanCetuximabEGFR protein, humanErbB ReceptorsKRAS protein, humanMicroRNAsMIRN425 microRNA, humanNeoplasm ProteinsPanitumumabProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Colorectal carcinoma, KRAS mutation, miR-425-5p expression levels, DICER1 gene, TNFRSF10B genePTEN gene.

Identifiers

PMID31673240
PMCPMC6818206
OpenAlexW2982686105

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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.