Compartment-specific multiomic profiling identifies SRC and GNAS as candidate drivers of epithelial-to-mesenchymal transition in ovarian carcinosarcoma Article Swipe
C. Simon Herrington
,
Ailsa J. Oswald
,
Lorna J. Stillie
,
Ian Croy
,
Michael Churchman
,
Robert L. Hollis
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1038/s41416-023-02508-3
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1038/s41416-023-02508-3
Background Ovarian carcinosarcoma (OCS) is an exceptionally aggressive and understudied ovarian cancer type harbouring distinct carcinomatous and sarcomatous compartments. Here, we seek to identify shared and compartment-specific events that may represent potential therapeutic targets and candidate drivers of sarcomatous compartment formation through epithelial-to-mesenchymal transition (EMT). Methods We performed multiomic profiling (exome sequencing, RNA-sequencing, microRNA profiling) of paired carcinomatous and sarcomatous components in 12 OCS cases. Results While paired sarcomatous and carcinomatous compartments demonstrate substantial genomic similarities, multiple loci are recurrently copy number-altered between components; regions containing GNAS and SRC are recurrently gained within the sarcomatous compartment. CCNE1 gain is a common event in OCS, occurring more frequently than in high grade serous ovarian carcinoma (HGSOC). Transcriptomic analysis suggests increased MAPK activity and subtype switching toward poor prognosis HGSOC-derived transcriptomic subtypes within the sarcomatous component. The two compartments show global differences in microRNA profiles, with differentially expressed microRNAs targeting EMT-related genes ( SIRT1 , ZEB2 ) and regulators of pro-tumourigenic pathways (TGFβ, NOTCH); chrX is a highly enriched target of these microRNAs and is also frequently deleted across samples. The sarcomatous component harbours significantly fewer CD8-positive cells, suggesting poorer immune engagement. Conclusion CCNE1 gain and chrX loss are frequent in OCS. SRC gain, increased GNAS expression and microRNA dysregulation represent potential mechanisms driving sarcomatous compartment formation.
Related Topics
Concepts
Biology
Stathmin
Transcriptome
microRNA
Cancer research
Epithelial–mesenchymal transition
Carcinosarcoma
Gene expression profiling
Serous fluid
Ovarian cancer
Cancer
Carcinoma
Gene
Genetics
Gene expression
Metastasis
Biochemistry
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1038/s41416-023-02508-3
- https://www.nature.com/articles/s41416-023-02508-3.pdf
- OA Status
- hybrid
- Cited By
- 5
- References
- 47
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4389735013
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4389735013Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1038/s41416-023-02508-3Digital Object Identifier
- Title
-
Compartment-specific multiomic profiling identifies SRC and GNAS as candidate drivers of epithelial-to-mesenchymal transition in ovarian carcinosarcomaWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-12-14Full publication date if available
- Authors
-
C. Simon Herrington, Ailsa J. Oswald, Lorna J. Stillie, Ian Croy, Michael Churchman, Robert L. HollisList of authors in order
- Landing page
-
https://doi.org/10.1038/s41416-023-02508-3Publisher landing page
- PDF URL
-
https://www.nature.com/articles/s41416-023-02508-3.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
hybridOpen access status per OpenAlex
- OA URL
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https://www.nature.com/articles/s41416-023-02508-3.pdfDirect OA link when available
- Concepts
-
Biology, Stathmin, Transcriptome, microRNA, Cancer research, Epithelial–mesenchymal transition, Carcinosarcoma, Gene expression profiling, Serous fluid, Ovarian cancer, Cancer, Carcinoma, Gene, Genetics, Gene expression, Metastasis, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
5Total citation count in OpenAlex
- Citations by year (recent)
-
2024: 5Per-year citation counts (last 5 years)
- References (count)
-
47Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.analysis | 117 |
| abstract_inverted_index.distinct | 15 |
| abstract_inverted_index.enriched | 167 |
| abstract_inverted_index.frequent | 198 |
| abstract_inverted_index.harbours | 182 |
| abstract_inverted_index.identify | 24 |
| abstract_inverted_index.microRNA | 54, 142, 207 |
| abstract_inverted_index.multiple | 77 |
| abstract_inverted_index.pathways | 160 |
| abstract_inverted_index.samples. | 178 |
| abstract_inverted_index.subtypes | 130 |
| abstract_inverted_index.suggests | 118 |
| abstract_inverted_index.candidate | 36 |
| abstract_inverted_index.carcinoma | 114 |
| abstract_inverted_index.component | 181 |
| abstract_inverted_index.expressed | 146 |
| abstract_inverted_index.formation | 41 |
| abstract_inverted_index.increased | 119, 203 |
| abstract_inverted_index.microRNAs | 147, 171 |
| abstract_inverted_index.multiomic | 49 |
| abstract_inverted_index.occurring | 105 |
| abstract_inverted_index.performed | 48 |
| abstract_inverted_index.potential | 32, 210 |
| abstract_inverted_index.profiles, | 143 |
| abstract_inverted_index.profiling | 50 |
| abstract_inverted_index.prognosis | 127 |
| abstract_inverted_index.represent | 31, 209 |
| abstract_inverted_index.switching | 124 |
| abstract_inverted_index.targeting | 148 |
| abstract_inverted_index.Background | 1 |
| abstract_inverted_index.Conclusion | 191 |
| abstract_inverted_index.aggressive | 8 |
| abstract_inverted_index.component. | 134 |
| abstract_inverted_index.components | 61 |
| abstract_inverted_index.containing | 86 |
| abstract_inverted_index.expression | 205 |
| abstract_inverted_index.formation. | 215 |
| abstract_inverted_index.frequently | 107, 175 |
| abstract_inverted_index.harbouring | 14 |
| abstract_inverted_index.mechanisms | 211 |
| abstract_inverted_index.profiling) | 55 |
| abstract_inverted_index.regulators | 157 |
| abstract_inverted_index.suggesting | 187 |
| abstract_inverted_index.transition | 44 |
| abstract_inverted_index.EMT-related | 149 |
| abstract_inverted_index.compartment | 40, 214 |
| abstract_inverted_index.components; | 84 |
| abstract_inverted_index.demonstrate | 73 |
| abstract_inverted_index.differences | 140 |
| abstract_inverted_index.engagement. | 190 |
| abstract_inverted_index.recurrently | 80, 91 |
| abstract_inverted_index.sarcomatous | 18, 39, 60, 69, 95, 133, 180, 213 |
| abstract_inverted_index.sequencing, | 52 |
| abstract_inverted_index.substantial | 74 |
| abstract_inverted_index.therapeutic | 33 |
| abstract_inverted_index.CD8-positive | 185 |
| abstract_inverted_index.compartment. | 96 |
| abstract_inverted_index.compartments | 72, 137 |
| abstract_inverted_index.understudied | 10 |
| abstract_inverted_index.HGSOC-derived | 128 |
| abstract_inverted_index.carcinomatous | 16, 58, 71 |
| abstract_inverted_index.compartments. | 19 |
| abstract_inverted_index.dysregulation | 208 |
| abstract_inverted_index.exceptionally | 7 |
| abstract_inverted_index.significantly | 183 |
| abstract_inverted_index.similarities, | 76 |
| abstract_inverted_index.Transcriptomic | 116 |
| abstract_inverted_index.carcinosarcoma | 3 |
| abstract_inverted_index.differentially | 145 |
| abstract_inverted_index.number-altered | 82 |
| abstract_inverted_index.transcriptomic | 129 |
| abstract_inverted_index.RNA-sequencing, | 53 |
| abstract_inverted_index.pro-tumourigenic | 159 |
| abstract_inverted_index.compartment-specific | 27 |
| abstract_inverted_index.epithelial-to-mesenchymal | 43 |
| cited_by_percentile_year.max | 98 |
| cited_by_percentile_year.min | 97 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 6 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/1 |
| sustainable_development_goals[0].score | 0.7900000214576721 |
| sustainable_development_goals[0].display_name | No poverty |
| citation_normalized_percentile.value | 0.84872958 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |