Evidence map›Paper›PMID 37894914›Full record

ArticleInternational journal of molecular sciences2023

Assessing the Potential of Small Peptides for Altering Expression Levels of the Iron-Regulatory Genes

Crawford Currie, Christian Bjerknes, Tor Åge Myklebust, Bomi Framroze

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-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

8 citing papers in PubMed, 8 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

4 authors at 3 institutions in 2 countries.

Crawford CurrieHBC Immunology Inc., 1455 Adams Drive, Suite, Menlo Park, CA 2043, USA.ORCID 0000-0002-4441-5262
Christian BjerknesHofseth Biocare, Keiser Wilhelmsgate 24, 6003 Ålesund, Norway.
Tor Åge MyklebustDepartment of Registration, Cancer Registry of Norway, 0379 Oslo, Norway.ORCID 0000-0003-4645-1635
Bomi FramrozeHBC Immunology Inc., 1455 Adams Drive, Suite, Menlo Park, CA 2043, USA.ORCID 0000-0002-5251-8982
Menlo School · USÅlesund Hospital · NONorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent research highlights the key role of iron dyshomeostasis in the pathogenesis of prostate cancer (PCa). PCa cells are heavily dependent on bioavailable iron, which frequently results in the reprogramming of iron uptake and storage pathways. Although advanced-stage PCa is currently incurable, bioactive peptides capable of modulating key iron-regulatory genes may constitute a means of exploiting a metabolic adaptation necessary for tumor growth. Recent annual increases in PCa incidence have been reported, highlighting the urgent need for novel treatments. We examined the ability of LNCaP, PC3, VCaP, and VCaP-EnzR cells to form colonies in the presence of androgen receptor inhibitors (ARI) and a series of iron-gene modulating oligopeptides (FT-001-FT-008). The viability of colonies following treatment was determined with clonogenic assays, and the expression levels of

Indexed as

Prostatic NeoplasmsReceptors, AndrogenAndrogensCell Line, TumorFerritinsGenes, RegulatorHumansIronMaleOxidoreductasesPeptidesReceptors, TransferrinAndrogensFerritinsFTH1 protein, humanIronOxidoreductasesPeptidesReceptors, AndrogenReceptors, Transferrinanticancer peptidesbioactive oligopeptideschemosensitizationFTH1 modulationiron metabolismiron regulating peptidesprostate cancer

Identifiers

PMID37894914
PMCPMC10607736
OpenAlexW4387668053

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.