Evidence map›Paper›PMID 30995246›Full record

ArticlePloS one2019

Critical role of miR-10b in B-RafV600E dependent anchorage independent growth and invasion of melanoma cells.

Ila Datar, Gardiyawasam Kalpana, Jungmin Choi, Tupa Basuroy, Robert Trumbly, Sri Krishna Chaitanya Arudra, Michael D McPhee, Ivana de la Serna, Kam C Yeung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. 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

9 authors at 5 institutions in 1 country.

Ila DatarCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH, United States of America.
Gardiyawasam KalpanaDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, OH, United States of America.
Jungmin ChoiDepartment of Genetics, Yale School of Medicine, New Haven, CT, United States of America.
Tupa BasuroyDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, OH, United States of America.
Robert TrumblyDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, OH, United States of America.
Sri Krishna Chaitanya ArudraDepartment of Pathology, Sanford Hospital, Bismarck, ND, United States of America.
Michael D McPheeProMedica Cancer Institute, Toledo, OH, United States of America.
Ivana de la SernaDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, OH, United States of America.
Kam C YeungDepartment of Cancer Biology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, OH, United States of America.ORCID 0000-0002-1415-484X
University of Toledo · USCase Western Reserve University · USProMedica Russell J. Ebeid Children's Hospital · USSanford Medical Center · USYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent high-throughput-sequencing of cancer genomes has identified oncogenic mutations in the B-Raf genetic locus as one of the critical events in melanomagenesis. B-Raf encodes a serine/threonine kinase that regulates the MAPK/ERK kinase (MEK) and extracellular signal-regulated kinase (ERK) protein kinase cascade. In normal cells, the activity of B-Raf is tightly regulated and is required for cell growth and survival. B-Raf gain-of-function mutations in melanoma frequently lead to unrestrained growth, enhanced cell invasion and increased viability of cancer cells. Although it is clear that the invasive phenotypes of B-Raf mutated melanoma cells are stringently dependent on B-Raf-MEK-ERK activation, the downstream effector targets that are required for oncogenic B-Raf-mediated melanomagenesis are not well defined. miRNAs have regulatory functions towards the expression of genes that are important in carcinogenesis. We observed that miR-10b expression correlates with the presence of the oncogenic B-Raf (B-RafV600E) mutation in melanoma cells. While expression of miR-10b enhances anchorage-independent growth of B-Raf wild-type melanoma cells, miR-10b silencing decreases B-RafV600E cancer cell invasion in vitro. Importantly, the expression of miR-10b is required for B-RafV600E-mediated anchorage independent growth and invasion of melanoma cells in vitro. Taken together our results suggest that miR-10b is an important mediator of oncogenic B-RafV600E activity in melanoma.

Indexed as

Gain of Function MutationGene Expression Regulation, NeoplasticAmino Acid SubstitutionCell Line, TumorCell SurvivalHumansMAP Kinase Signaling SystemMelanomaMicroRNAsMutation, MissenseNeoplasm InvasivenessProto-Oncogene Proteins B-rafRNA, NeoplasmBRAF protein, humanMicroRNAsMIRN10 microRNA, humanProto-Oncogene Proteins B-rafRNA, Neoplasm

Identifiers

PMID30995246
PMCPMC6469749
OpenAlexW2953314816

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.