Ovarian Cancer Dynamics
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR303411.fastq.gz | Fastqsanger.gz | |||
| ERR303412.fastq.gz | Fastqsanger.gz | |||
| ERR303413.fastq.gz | Fastqsanger.gz | |||
| ERR303414.fastq.gz | Fastqsanger.gz | |||
| ERR303415.fastq.gz | Fastqsanger.gz |
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Project description:Mitochondria are dynamic organelles that are important for cell growth and proliferation. Dysregulated mitochondrial dynamics are highly associated with the initiation and progression of various cancers, including ovarian cancer. However, the regulatory mechanism underlying mitochondrial dynamics is still not fully understood. Previously, our study showed that carnitine palmitoyltransferase 1A (CPT1A) is highly expressed in ovarian cancer cells and promotes the development of ovarian cancer. Here, we find that CPT1A regulates mitochondrial dynamics and promotes mitochondrial fission in ovarian cancer cells. Our study futher shows that CPT1A regulates mitochondrial fission and function through mitochondrial fission factor (MFF) to promote the growth and proliferation of ovarian cancer cells. Mechanistically, we show that CPT1A promotes succinylation of MFF at lysine 302 (K302), which protects against Parkin-mediated ubiquitin-proteasomal degradation of MFF. Finally, the study shows that MFF is highly expressed in ovarian cancer cells and that high MFF expression is associated with poor prognosis in patients with ovarian cancer. MFF inhibition significantly inhibits the progression of ovarian cancer in vivo. Overall, CPT1A regulates mitochondrial dynamics through MFF succinylation to promote the development of ovarian cancer. Moreover, our findings suggest that MFF is a potential therapeutic target for ovarian cancer.
2023-05-15 | PXD041990 | Pride
Project description:We reveal three-dimensional patterns of tumour growth by exploiting the unique metastasizing patterns of treatment naïve stage IIIC/IV epithelial ovarian cancer. We performed topographic mapping of structural genomic rearrangements, coding mutations, copy number changes and RNA expression in biopsies derived from 27 primary and metastatic sites across three patients. Based on somatic genomic changes, we performed sample clustering and obtained unique insight in natural tumour growth and spread. Based on extensive multi-level profiling, our data highlight the diverse modes of epithelial ovarian cancer development before applying selective pressure from therapy.
2013-06-05 | GSE47633 | GEO
Project description:We reveal three-dimensional patterns of tumour growth by exploiting the unique metastasizing patterns of treatment naïve stage IIIC/IV epithelial ovarian cancer. We performed topographic mapping of structural genomic rearrangements, coding mutations, copy number changes and RNA expression in biopsies derived from 27 primary and metastatic sites across three patients. Based on somatic genomic changes, we performed sample clustering and obtained unique insight in natural tumour growth and spread. Based on extensive multi-level profiling, our data highlight the diverse modes of epithelial ovarian cancer development before applying selective pressure from therapy. We performed SNP array analysis on tumor biopsies from 3 patients (P1, P2, P3) with advanced stage ovarian cancer. This submission includes SNP data for 26 tumor biopsies and 5 normal tissue samples.
2013-06-05 | E-GEOD-47633 | biostudies-arrayexpress
Project description:Ovarian cancer is also known as a silent killer as women are usually diagnosed in advanced stages when the disease has already spread to vital peritoneal organs leading to poor survival. Therefore, improving outcomes for this disease would require a greater understanding of the earliest stages, where the disease can be cured with current treatments. Fallopian tubes (FTs) are a site of origin of ovarian cancer. Here, by combining gene sequencing, proteomics, organoids, mouse genetics, lineage tracing, and quantitative modeling, we showed that mutant Pax8+ FT progenitor cells gain clonal growth advantage over their wild-type neighbors and expand over time, colonizing large areas of FT epithelium, resulting in the formation of pre-cancerous lesions. The growth of these precursor lesions is modulated by ovarian hormones, where estrogen promotes and progesterone suppresses their growth. Collectively, this study provides insight into how a single mutant FT epithelial cell leads to early ovarian cancer evolution.
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Project description:Background. Genome-wide expression changes are associated with development of chemoresistance in patients with ovarian cancer (OVCA); the BCL2 antagonist of cell death (BAD) apoptosis pathway may play a role in clinical outcome. Methods. We analyzed specimens and/or genomic data from 1,406 patients and 116 cancer cell lines. Genome-wide expression changes and cisplatin-resistance were evaluated in OVCA cell lines subjected to a total of 144 (cisplatin)-treatment/recovery cycles. Pathway analysis was performed on genes associated with increasing cisplatin-resistance. BAD protein phosphorylation was studied in patient samples and cell lines, and small interfering RNAs (siRNA) used to explore the pathway as a therapeutic target. We evaluated the influence of BAD-pathway expression on chemosensitivity and/or clinical outcome using genomic data from 60 human cancer cell lines and ovarian, breast, colon, and brain cancers from 1,258 patients. Results. The BAD pathway was associated with evolution of OVCA cell line cisplatin-resistance (P<0.001) and resistance of 7 human cancer cell types to 8 cytotoxic agents (P<0.05). OVCA chemoresistance was associated with BAD protein phosphorylation, and targeted siRNA modulation produced corresponding changes in chemosensitivity. Expression of a 47-gene BAD-pathway signature was associated with survival of 1,258 patients with ovarian, breast, colon, and brain cancer. The OVCA BAD-pathway signature survival advantage was independent of surgical cytoreductive status. Conclusions. The BAD apoptosis pathway influences the sensitivity of human cancers to a variety of chemotherapies, likely via modulation of BAD-phosphorylation. The pathway has clinical relevance as a potential biomarker of therapeutic response, patient survival, and as a promising therapeutic target. Twenty-eight (28) advanced-stage serous epithelial ovarian cancers were resected at the time of primary surgery from patients who would receive platinum-based therapy. The tumors were arrayed on Affymetrix HG-U133A GeneChips. The samples were analyzed with respect to the BAD pathway for correlation to overall survival and cisplatin response.
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2014-10-02 | E-GEOD-50831 | biostudies-arrayexpress
Project description:Spheroid formation during epithelial ovarian cancer progression correlates with peritoneal organ colonization, disease recurrence, and poor prognosis. Although cancer progression has been demonstrated to be associated with and driven by metabolic changes within transformed cells, possible associations between metabolic dynamics and metastatic morphological transitions remain unexplored. To address this problem, performed quantitative proteomics was performed to identify protein signatures associated with three distinct morphologies (2D monolayers and two geometrically individual three-dimensional spheroidal states) of the high-grade serous ovarian cancer line OVCAR-3. Integrating the protein states into genome-scale metabolic models allowed the construction of context-specific metabolic models for each morphological stage of the OVCAR-3 cell line and systematically evaluate their metabolic functionalities.
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