ArticleCancer research2010
Deficiency of splicing factor 1 suppresses the occurrence of testicular germ cell tumors.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Phenotype and gene signature of testicular tumors in 129.MOLF-Chr19 mice resemble human teratomas.Andrology · 2025Article
- Teratoma Development in 129.MOLF-Chr19 Mice Elicits Two Waves of Immune Cell Infiltration.International journal of molecular sciences · 2024Article
- Commitment Complex Splicing Factors in Cancers of the Gastrointestinal Tract-An In Silico Study.Bioinformatics and biology insights · 2024Article
- The distinct roles of zinc finger CCHC-type (ZCCHC) superfamily proteins in the regulation of RNA metabolism.RNA biology · 2021Review
- Non-Coding RNAs and Splicing Activity in Testicular Germ Cell Tumors.Life (Basel, Switzerland) · 2021Review
- Article
- Systematic characterization of the branch point binding protein, splicing factor 1, gene family in plant development and stress responses.BMC plant biology · 2020Article
- Knockdown of lncRNA MIAT inhibits proliferation and cisplatin resistance in non-small cell lung cancer cells by increasing miR-184 expression.Oncology letters · 2020Article
- Bioinformatics Analysis of Gene Expression Profiles for Risk Prediction in Patients with Septic Shock.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Survival associated alternative splicing events in diffuse large B-cell lymphoma.American journal of translational research · 2018Article
- LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression.Cancer medicine · 2017Article
- Germ cell tumors: Insights from the Drosophila ovary and the mouse testis.Molecular reproduction and development · 2017Review
- Contrasting genetic architectures in different mouse reference populations used for studying complex traits.Genome research · 2015Review
- Tumor loci and their interactions on mouse chromosome 19 that contribute to testicular germ cell tumors.BMC genetics · 2014Article
- Contrasting effects of Deadend1 (Dnd1) gain and loss of function mutations on allelic inheritance, testicular cancer, and intestinal polyposis.BMC genetics · 2013Article
- PTBP1-dependent regulation of USP5 alternative RNA splicing plays a role in glioblastoma tumorigenesis.Molecular carcinogenesis · 2012Article
- Chromosome substitution strains: gene discovery, functional analysis, and systems studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2012Review
- The protein kinase KIS impacts gene expression during development and fear conditioning in adult mice.PloS one · 2012Article
- Characterization of progression-related alternative splicing events in testicular germ cell tumors.Asian journal of andrologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Testicular germ cell tumors (TGCT) originate from germ cells. The 129-Ter and M19 (129.MOLF-Chr19 consomic) mouse strains have extremely high incidences of TGCTs. We found that the expression levels of Sf1-encoded splicing factor 1 (SF1) can modulate the incidence of TGCTs. We generated mice with inactivated Sf1. Sf1 null mice (Sf1-/-) died before birth. Mice with one intact allele of Sf1 (Sf1+/-) were viable but expressed reduced levels of Sf1. When Sf1-deficient mice (Sf1+/-) were crossed to the 129-Ter and M19 strains, we observed decreased incidence of TGCTs in Sf1+/-;Ter and Sf1+/-;M19/+ mice compared with that in control cohorts. Therefore, Sf1 deficiency protects against TGCT development in both strains. Sf1 is expressed in the testes. We found that Sf1 levels vary significantly in the testes of inbred strains such as 129 and MOLF, and as such Sf1 is an oncogenic tumor-susceptibility factor from 129. Our results also highlight the complications involved in evaluating Sf1 levels and TGCT incidences. When a large number of tumor-promoting factors are present in a strain, the protective effect of lower Sf1 levels is masked. However, when the dosage of tumor-promoting factors is reduced, the protective effect of lower Sf1 levels becomes apparent. SF1 is involved in splicing of specific pre-mRNAs in cells. Alternate splicing generates the complex proteosome in eukaryotic cells. Our data indicate that Sf1 levels in mouse strains correlate with their incidences of TGCTs and implicate the importance of splicing mechanisms in germ cell tumorigenesis.
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Registered trials
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