ArticleOncogene2009
Downregulation of SRF-FOS-JUNB pathway in fumarate hydratase deficiency and in uterine leiomyomas.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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.
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.
Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Spatial transcriptomics uncovers the hybrid molecular identity, ciliated phenotype, and immune signature of adenomyosis lesions.Science advances · 2026Article
- Article
- Evidence of a causal effect of genetic tendency to gain muscle mass on uterine leiomyomata.Nature communications · 2023Article
- Evidence-Based Management of Uterine Fibroids With Botanical Drugs-A Review.Frontiers in pharmacology · 2022Review
- β-RA Targets Mitochondrial Metabolism and Adipogenesis, Leading to Therapeutic Benefits against CoQ Deficiency and Age-Related Overweight.Biomedicines · 2021Article
- Epigenomic tensor predicts disease subtypes and reveals constrained tumor evolution.Cell reports · 2021Article
- Genetic variant of SRF-rearranged myofibroma with a misleading nuclear expression of STAT6 and STAT6 involvement as 3' fusion partner.Virchows Archiv : an international journal of pathology · 2021Article
- An Integrative Analysis of Transcriptome and GWAS Data to Identify Potential Candidate Genes Influencing Meat Quality Traits in Pigs.Frontiers in genetics · 2021Article
- Coenzyme Q10 modulates sulfide metabolism and links the mitochondrial respiratory chain to pathways associated to one carbon metabolism.Human molecular genetics · 2020Article
- Article
- Article
- Article
- Mitochondrial biogenesis is transcriptionally repressed in lysosomal lipid storage diseases.eLife · 2019Article
- Mitochondrial function - gatekeeper of intestinal epithelial cell homeostasis.Nature reviews. Gastroenterology & hepatology · 2018Review
- Mitochondrial adventures at the organelle society.Biochemical and biophysical research communications · 2018Review
- Screening of potential biomarkers in uterine leiomyomas disease via gene expression profiling analysis.Molecular medicine reports · 2018Article
- Protein profiling of blood samples from patients with hereditary leiomyomatosis and renal cell cancer by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry.International journal of molecular sciences · 2012Article
- Article
- Revisiting the TCA cycle: signaling to tumor formation.Trends in molecular medicine · 2011Review
- Inborn and acquired metabolic defects in cancer.Journal of molecular medicine (Berlin, Germany) · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defects of metabolic enzymes result in a variety of manifestations not logically explained by the primary metabolic function. Dominant defects of fumarate hydratase (FH) result in predisposition to cutaneous and uterine leiomyomas, and renal cell cancer. FH is a metabolic enzyme of the tricarboxylic acid cycle, and its tumor-suppressor mechanism is not fully understood. We compared the consequences of FH deficiency and respiratory chain (RC) deficiency using global expression pattern of diploid primary fibroblasts. This approach utilized the information that RC defects do not seem to predispose to tumorigenesis, and the aim was to identify FH-specific signaling effects that might have relevance to tumor formation. These results were then compared to global expression patterns of FH-deficient and sporadic uterine leiomyoma data sets. We show here that FH-deficient fibroblasts share a common transcriptional fingerprint with FH-deficient and sporadic leiomyomas, highlighting the downregulation of serum response factor (SRF)-regulated transcripts, particularly the FOS-JUNB pathway. We confirmed the downregulation of this pathway at transcriptional and protein level. SRF has a fundamental function in the differentiation of smooth muscle progenitor cells, and its downregulation both in diploid FH-deficient primary fibroblasts and in leiomyomas suggests an early function in the mechanism of uterine leiomyoma formation in FH deficiency. Concordantly, the phosphorylated form of SRF, known to activate transcription, is undetectable in leiomyomas whereas clearly detected in several nuclei in the differentiated myometrium. A similar transcriptional SRF-pathway fingerprint in FH-deficient and sporadic leiomyomas emphasizes the potential importance of this pathway in primary events leading to leiomyomatosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.