Evidence map›Paper›PMID 35482254›Full record

ArticleMetabolomics : Official journal of the Metabolomic Society2022

Establishing pteridine metabolism in a progressive isogenic breast cancer cell model - part II.

Lindsey Rasmussen, Zachary Foulks, Jiandong Wu, Casey Burton, Honglan Shi

Open access · greenAbstract read
In one paragraph

Article in Metabolomics : Official journal of the Metabolomic Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Trial
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

5 authors at 1 institution in 1 country.

Lindsey RasmussenDepartment of Chemistry, Missouri University of Science and Technology, 400 W 11th Street, 65409, Rolla, MO, USA.
Zachary FoulksDepartment of Chemistry, Missouri University of Science and Technology, 400 W 11th Street, 65409, Rolla, MO, USA.
Jiandong WuDepartment of Chemical and Biochemical Engineering, Missouri University of Science and Technology, 65409, Rolla, MO, USA.
Casey BurtonDepartment of Chemistry, Missouri University of Science and Technology, 400 W 11th Street, 65409, Rolla, MO, USA. c.f.burton@mst.edu.
Honglan ShiDepartment of Chemistry, Missouri University of Science and Technology, 400 W 11th Street, 65409, Rolla, MO, USA. honglan@mst.edu.ORCID 0000-0002-0801-5683
Missouri University of Science and Technology · US

Funding

Establishing Biological Significance of Pteridine Metabolites in Progressive Breast CancerR03CA219337 · NCI · MISSOURI UNIVERSITY OF SCIENCE & TECHNOLOGY · PI BURTON, CASEY, MA, YINFA · 2019 to 2020
$155k
NCI NIH HHS R03 CA219337
6 · The paper itself

Abstract

introductionDetermining the biological significance of pteridines in cancer development and progression remains an important step in understanding the altered levels of urinary pteridines seen in certain cancers. Our companion study revealed that several folate-derived pteridines and lumazines correlated with tumorigenicity in an isogenic, progressive breast cancer cell model, providing direct evidence for the tumorigenic origin of pteridines.

objectivesThis study sought to elucidate the pteridine biosynthetic pathway in a progressive breast cancer model via direct pteridine dosing to determine how pteridine metabolism changes with tumorigenicity.

methodsFirst, MCF10AT breast cancer cells were dosed individually with 15 pteridines to determine which pteridines were being metabolized and what metabolic products were being produced. Second, pteridines that were significantly metabolized were dosed individually across the progressive breast cancer cell model (MCF10A, MCF10AT, and MCF10ACA1a) to determine the relationship between each metabolic reaction and breast cancer tumorigenicity.

resultsSeveral pteridines were found to have altered metabolism in breast cancer cell lines, including pterin, isoxanthopterin, xanthopterin, sepiapterin, 6-biopterin, lumazine, and 7-hydroxylumazine (p < 0.05). In particular, isoxanthopterin and 6-biopterin concentrations were differentially expressed (p < 0.05) with respect to tumorigenicity following dosing with pterin and sepiapterin, respectively. Finally, the pteridine biosynthetic pathway in breast cancer cells was proposed based on these findings.

conclusionsThis study, along with its companion study, demonstrates that pteridine metabolism becomes disrupted in breast cancer tumor cells. This work highlights several key metabolic reactions within the pteridine biosynthetic pathway that may be targeted for further investigation and clinical applications.

Indexed as

Breast NeoplasmsBiopterinsFemaleHumansMetabolomicsPteridinesPterinsBiopterinsPteridinesPterinsBiomarkerBreast cancerHPLC-MS/MSMCF10A cell linePteridinePteridine metabolism

Identifiers

PMID35482254
PMCPMC10030290
OpenAlexW4224998925

What OpenQuestion holds

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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.