Evidence map›Paper›PMID 25007054›Full record

ArticlePloS one2014

Evidence that RASSF1C stimulation of lung cancer cell proliferation depends on IGFBP-5 and PIWIL1 expression levels.

Mark E Reeves, Matthew Firek, Shin-Tai Chen, Yousef G Amaar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  3. The Role of RASSF1C in the Tumor Microenvironment.Current issues in molecular biology · 2023
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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

4 authors at 2 institutions in 1 country.

Mark E ReevesSurgical Oncology Laboratory, Loma Linda VA Medical Center, Loma Linda, California, United States of America; Department of Surgery, Loma Linda University School of Medicine, Loma Linda, California, United States of America.
Matthew FirekSurgical Oncology Laboratory, Loma Linda VA Medical Center, Loma Linda, California, United States of America.
Shin-Tai ChenMusculoskeletal Disease Center, Loma Linda VA Medical Center, Loma Linda, California, United States of America.
Yousef G AmaarSurgical Oncology Laboratory, Loma Linda VA Medical Center, Loma Linda, California, United States of America; Department of Surgery, Loma Linda University School of Medicine, Loma Linda, California, United States of America.
Loma Linda University Medical Center · USLoma Linda University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RASSF1C is a major isoform of the RASSF1 gene, and is emerging as an oncogene. This is in contradistinction to the RASSF1A isoform, which is an established tumor suppressor. We have previously shown that RASSF1C promotes lung cancer cell proliferation and have identified RASSF1C target genes with growth promoting functions. Here, we further report that RASSF1C promotes lung cancer cell migration and enhances lung cancer cell tumor sphere formation. We also show that RASSF1C over-expression reduces the inhibitory effects of the anti-cancer agent, betulinic acid (BA), on lung cancer cell proliferation. In previous work, we demonstrated that RASSF1C up-regulates piwil1 gene expression, which is a stem cell self-renewal gene that is over-expressed in several human cancers, including lung cancer. Here, we report on the effects of BA on piwil1 gene expression. Cells treated with BA show decreased piwil1 expression. Also, interaction of IGFBP-5 with RASSF1C appears to prevent RASSF1C from up-regulating PIWIL1 protein levels. These findings suggest that IGFBP-5 may be a negative modulator of RASSF1C/ PIWIL1 growth-promoting activities. In addition, we found that inhibition of the ATM-AMPK pathway up-regulates RASSF1C gene expression.

Indexed as

Gene ExpressionAntineoplastic AgentsArgonaute Proteinsbeta CateninBetulinic AcidCell MovementCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansHydroxamic AcidsInsulin-Like Growth Factor Binding Protein 5Lung NeoplasmsPentacyclic TriterpenesPyrazolesPyrimidinesAntineoplastic AgentsArgonaute Proteinsbeta CateninBetulinic AcidCTNNB1 protein, humandorsomorphinHydroxamic AcidsInsulin-Like Growth Factor Binding Protein 5Pentacyclic TriterpenesPIWIL1 protein, humanPyrazolesPyrimidinesRASSF1 protein, humantrichostatin ATriterpenesTumor Suppressor Proteins

Identifiers

PMID25007054
PMCPMC4090148
OpenAlexW2064397865

What OpenQuestion holds

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LicenceCC0
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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.