ArticleOncogene2013
Adult ovarian granulosa cell tumor transcriptomics: prevalence of FOXL2 target genes misregulation gives insights into the pathogenic mechanism of the p.Cys134Trp somatic mutation.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 60 citations in OpenAlex.
- Regulation of murine follicle-stimulating hormone β subunit transcription by newly identified enhancers.Endocrinology · 2026Article
- Regulation of murine follicle-stimulating hormone β subunit transcription by newly identified enhancers.bioRxiv : the preprint server for biology · 2025Article
- Gain-of-Function Chromatin Remodeling Activity of Oncogenic FOXL2C134W Reprograms Glucocorticoid Receptor Occupancy to Drive Granulosa Cell Tumors.Cancer research · 2025Article
- A cellular model provides insights into the pathogenicity of the oncogenic FOXL2 somatic variant p.Cys134Trp.British journal of cancer · 2024Article
- A matter of new life and cell death: programmed cell death in the mammalian ovary.Journal of biomedical science · 2024Review
- Analysis of Non-Relapsed and Relapsed Adult Type Granulosa Cell Tumors Suggests Stable Transcriptomes during Tumor Progression.Current issues in molecular biology · 2022Article
- The Role of Omics Approaches to Characterize Molecular Mechanisms of Rare Ovarian Cancers: Recent Advances and Future Perspectives.Biomedicines · 2021Review
- FOXO1 mitigates the SMAD3/FOXL2Journal of translational medicine · 2021Article
- Constitutive expression of progesterone receptor isoforms promotes the development of hormone-dependent ovarian neoplasms.Science signaling · 2020Article
- Mutant FOXL2Cancer research · 2020Article
- Review
- Article
- FOXO1 Negates the Cooperative Action of FOXL2Journal of the Endocrine Society · 2019Article
- New STAT3-FOXL2 pathway and its function in cancer cells.BMC molecular and cell biology · 2019Article
- FOXL2C134W-Induced CYP19 Expression via Cooperation With SMAD3 in HGrC1 Cells.Endocrinology · 2018Article
- FOXL2 molecular status in adult granulosa cell tumors of the ovary: A study of primary and metastatic cases.Oncology letters · 2016Article
- The four and a half LIM domains 2 (FHL2) regulates ovarian granulosa cell tumor progression via controlling AKT1 transcription.Cell death & disease · 2016Article
- Article
- Molecular manipulation of keratin 8/18 intermediate filaments: modulators of FAS-mediated death signaling in human ovarian granulosa tumor cells.Journal of ovarian research · 2016Article
- FOXO1/3 and PTEN Depletion in Granulosa Cells Promotes Ovarian Granulosa Cell Tumor Development.Molecular endocrinology (Baltimore, Md.) · 2015Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian granulosa cell tumors (OGCT) are the most frequent kind of sex cord-stromal tumors, and represent ∼2-5% of all ovarian malignancies. OGCTs exist as two entities, juvenile and adult types, with specific clinical and pathological characteristics. The molecular pathogenesis of these tumors has just begun to be unraveled. Indeed, recent studies have indicated that mutation and/or misregulation of the key ovarian transcription factor FOXL2 has a role in OGCT formation, although the mechanisms remain unclear. To better understand the molecular characteristics of OGCT, we studied the transcriptomic profiles of ten human adult-type OGCT samples, as well as ethnically matched granulosa cell (GC) controls. We find that the OGCT samples analyzed herein exhibit several hallmarks of cancer, including increased expression of genes linked to cell proliferation, but decreased expression of those conferring sensitivity to cell death. Moreover, genes differentially expressed in OGCTs are significantly enriched for known FOXL2 target genes, consistently with the prevalence of FOXL2 somatic mutation in these tumors. Expression of these targets is altered in a way expected to promote malignant transformation, for instance, through induction of genes associated with faster cell cycling and downregulation of genes associated with cell death. Over time, such defects may be responsible at least partly for the malignant transformation of healthy GCs into OGCT. These insights into the molecular pathogenesis of OGCTs may open the way to new efforts in the development of more targeted therapeutic strategies for OGCT patients.
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