Evidence map›Paper›PMID 28863773›Full record

ArticleBMC cancer2017

Down-regulation of miRNA-148a and miRNA-625-3p in colorectal cancer is associated with tumor budding.

Edita Baltruskeviciene, Diana Schveigert, Vaidotas Stankevicius, Ugnius Mickys, Tadas Zvirblis, Jaroslav Bublevic, Kestutis Suziedelis, Eduardas Aleknavicius

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

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  14. MicroRNA: Another Pharmacological Avenue for Colorectal Cancer?Frontiers in cell and developmental biology · 2020
    Review
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  16. Novel Multiple miRNA-Based Signatures for Predicting Overall Survival and Recurrence-Free Survival of Colorectal Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2019
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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

8 authors at 2 institutions in 1 country.

Edita BaltruskevicieneDepartament of medical oncology, National Cancer Institute, Santariskiu 1, 08660, Vilnius, LT, Lithuania. edita.baltruskeviciene@nvi.lt.
Diana SchveigertLaboratory of Molecular Oncology, National Cancer Institute, Vilnius, Lithuania.
Vaidotas StankeviciusLaboratory of Molecular Oncology, National Cancer Institute, Vilnius, Lithuania.
Ugnius MickysNational Center of Pathology, affiliate of Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania.
Tadas ZvirblisHematology, oncology and transfusiology center, Vilnius University Hospital Santaros Klinikos, Vilnius, Lithuania.
Jaroslav BublevicDepartament of medical oncology, National Cancer Institute, Santariskiu 1, 08660, Vilnius, LT, Lithuania.
Kestutis SuziedelisLaboratory of Molecular Oncology, National Cancer Institute, Vilnius, Lithuania.
Eduardas AleknaviciusDepartament of medical oncology, National Cancer Institute, Santariskiu 1, 08660, Vilnius, LT, Lithuania.
National Cancer Institute · LTVilnius University · LT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMiRNAs are often deregulated in colorectal cancer and might function as tumor suppressors or as oncogenes. They participate in controlling key signaling pathways involved in proliferation, invasion and apoptosis and may serve as prognostic and predictive markers. In this study we aimed to evaluate the role of miRNA-148a and miRNA-625-3p in metastatic colorectal cancer.

methodsFifty-four patients with a first-time diagnosed CRC receiving FOLFOX ± Bevacizumab were involved in the study. Tumor samples underwent routine pathology examination including evaluation for tumor budding and KRAS. MiRNA-148a and miRNA-625-3p expression analysis was done by RT-PCR. Associations between expression of both miRNAs and clinico-pathological factors, treatment outcomes and survival were analyzed.

resultsBoth miRNA-148a and miRNA-625-3p were down-regulated in the tumors compared to normal colonic mucosa. Significantly lower expression of both miRNAs was noticed in tumors with budding phenomenon compared to tumors without it (median values of miRNA-148a were 0.314 and 0.753 respectively, p = 0.011, and 0.404 and 0.620 respectively for miRNA-625-3p, p = 0.036). Significantly lower expression of miRNA-625-3p was detected in rectal tumors, compared to tumors in the colon (median 0.390 and 0.665 respectively, p = 0.037). Progression free survival was significantly lower in patients with high miRNA-148a expression (6 and 9 months respectively, p = 0.033), but there were no significant differences in PFS for miRNA-625-3p and in overall survival for both miRNAs.

conclusionsThere was a significant relationship between low miRNA-148a and miRNA-625-3p expression and tumor budding, which is thought to represent epithelial-mesenchymal transition. Both studied miRNAs may be associated with a more aggressive phenotype and could be the potential prognostic and predictive biomarkers in CRC. Further investigation is needed to confirm miRNAs involvement in EMT, and their prognostic and predictive value.

Indexed as

AgedBiomarkers, TumorColorectal NeoplasmsDisease-Free SurvivalEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMicroRNAsMiddle AgedOrganoplatinum CompoundsOxaliplatinPrognosisBiomarkers, TumorMicroRNAsMIRN148 microRNA, humanMIRN625 microRNA, humanOrganoplatinum CompoundsOxaliplatinColorectal cancermicroRNAMiRNA-148amiRNA-625-3pOxaliplatinTumor budding

Identifiers

PMID28863773
PMCPMC5580437
OpenAlexW2753900230

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.