Evidence map›Paper›PMID 38722825›Full record

ArticlePLoS genetics2024

Resf1 is a compound G4 quadruplex-associated tumor suppressor for triple negative breast cancer.

Megan R Majocha, Devin E Jackson, Ngoc-Han Ha, Ruhul Amin, Marie Pangrácová, Christina R Ross, Howard H Yang, Maxwell P Lee, Kent W Hunter

Abstract read
In one paragraph

Article in PLoS genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. 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.

Megan R MajochaLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0009-0006-7378-7408
Devin E JacksonLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Ngoc-Han HaLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Ruhul AminLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0001-8826-4040
Marie PangrácováLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0003-4184-4296
Christina R RossLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Howard H YangLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0002-9291-631X
Maxwell P LeeLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0003-3738-1292
Kent W HunterLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID 0000-0001-5963-8808

Funding

Genetic Modifiers of Intitiation and Progression of Mammary CancerZIABC011255 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUNTER, KENT WILLIAM · 2010 to 2025
$33.2M
Integrated analyses of genetics, epigenetics, and gene expressionZIHBC011703 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LEE, MAXWELL · 2016 to 2025
$10.9M
Intramural NIH HHS ZIA BC011255
6 · The paper itself

Abstract

Patients with ER-negative breast cancer have the worst prognosis of all breast cancer subtypes, often experiencing rapid recurrence or progression to metastatic disease shortly after diagnosis. Given that metastasis is the primary cause of mortality in most solid tumors, understanding metastatic biology is crucial for effective intervention. Using a mouse systems genetics approach, we previously identified 12 genes associated with metastatic susceptibility. Here, we extend those studies to identify Resf1, a poorly characterized gene, as a novel metastasis susceptibility gene in ER- breast cancer. Resf1 is a large, unstructured protein with an evolutionarily conserved intron-exon structure, but with poor amino acid conservation. CRISPR or gene trap mouse models crossed to the Polyoma Middle-T antigen genetically engineered mouse model (MMTV-PyMT) demonstrated that reduction of Resf1 resulted in a significant increase in tumor growth, a shortened overall survival time, and increased incidence and number of lung metastases, consistent with patient data. Furthermore, an analysis of matched tail and primary tissues revealed loss of the wildtype copy in tumor tissue, consistent with Resf1 being a tumor suppressor. Mechanistic analysis revealed a potential role of Resf1 in transcriptional control through association with compound G4 quadruplexes in expressed sequences, particularly those associated with ribosomal biogenesis. These results suggest that loss of Resf1 enhances tumor progression in ER- breast cancer through multiple alterations in both transcriptional and translational control.

Indexed as

Repressor ProteinsTriple Negative Breast NeoplasmsAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorG-QuadruplexesHumansLung NeoplasmsMiceNeoplasm MetastasisRepressor ProteinsResf1 protein, mouse

Identifiers

PMID38722825
PMCPMC11081379

What OpenQuestion holds

Textmetadata
LicenceCC0
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.