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MicroRNA sequencing for platinum-resistant high-grade serous ovarian carcinoma

ABSTRACT: Ovarian cancer is one of the leading causes of death in females in the world. High-grade serous ovarian carcinoma (HGSOC) is the most common histological subtype, and the platinum-resistance is a clinical challenge, In this study, we investigated the microRNA (miRNA) profiles of platinum-resistant and platinum-sensitive HGSOC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273635 | GEO | 2025/09/03

REPOSITORIES: GEO

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Gene expression profiles of platinum-resistant high-grade serous ovarian carcinoma

Project description:Ovarian cancer is one of the leading causes of death in females in the world. High-grade serous ovarian carcinoma (HGSOC) is the most common histological subtype, and platinum platinum-resistance is a clinical challenge, In this study, we investigated the gene expression profiles of platinum-resistant and platinum-sensitive HGSOC.

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Spatial transcriptomics for platinum-resistant high-grade serous ovarian carcinoma

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Transcriptomes of tumour-associated macrophages from high grade serous ovarian cancer pre- and post-platinum-based neoadjuvant chemotherapy.

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Proteomic analysis of tumor tissues form high-grade serous ovarian cancer patients

Project description:In the present project, in order to explore the molecular basis of platinum resistance and further determine potential biomarkers and therapeutic targets for high-grade serous ovarian cancer (HGSOC), we conducted a comparative proteomic analysis to identify the differentially expressed proteins between tumor tissues from platinum-sensitive and platinum-resistant HGSOC patient groups.

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Tumor Exosome-transmitted LncRNA CATED Promotes Platinum-resistant in High-grade Serous Ovarian Cancer

Project description:High-grade serous ovarian cancer (HGSOC) represents the most lethal type of gynecological cancer, with platinum resistance being a serious challenge in HGSOC treatment. Long non-coding RNA (lncRNA) plays critical regulatory roles in the occurrence and development of various cancers, including HGSOC. Here, using RNA sequencing of tumor exosomes from HGSOC patients, we identified lncRNA CATED was significantly upregulated in both tumors and tumor-derived exosomes in platinum-resistant HGSOC, and low CATED level correlated with good prognosis. Functionally, CATED enhanced cisplatin resistance via promoting cell proliferation and decreasing apoptosis both in vitro and in vivo. These effects could also be transferred via CATED-overexpressing exosomes from donor cells and tumor exosomes from HGSOC patients. Mechanistically, CATED bound to and upregulated DHX36 via PIAS1-mediated SUMOylation at K105 site, and elevated DHX36 increased the downstream RAP1A protein levels by enhancing RAP1A mRNA translation, consequently activating MAPK pathway to promote platinum resistance in HGSOC. ASO-mediated knockdown of CATED reversed the platinum resistance in exosome-transferring mouse models through DHX36-RAP1A-MAPK pathway. Overall, these findings offer new insights into the critical roles of exosomal lncRNAs in platinum resistance, and indicate that CATED may be a potential target of HGSOC treatment.

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Multiomic analysis identifies CPT1A as a potential therapeutic target in platinum-refractory high grade serous ovarian cancer

Project description:Platinum-based chemotherapies are widely used anti-cancer drugs. Tumor resistance to platinum compounds is a major determinant of patient survival, including in high grade serous ovarian cancer (HGSOC). To understand mechanisms of platinum resistance and identify potential therapeutic targets in resistant HGSOC, we generated a comprehensive, reproducible data resource comprised of dynamic (+/-carboplatin) proteomic/posttranslational modification and RNASeq profiles from HGSOC intra-patient cell line pairs derived from 3 patients before and after acquiring platinum resistance. The molecular profiles revealed extensive responses to carboplatin and differential responses between sensitive and resistant cells. Higher oxidative phosphorylation and fatty acid oxidation (FAO) pathway expression were observed in the platinum-resistant cells, which was further validated in patient-derived xenograft (PDX) models. We show that both pharmacologic inhibition and CRISPR knockout of CPT1A, which represents a rate limiting step of FAO, sensitize HGSOC cells to platinum. Thus, FAO is a candidate therapeutic target to overcome platinum resistance.

2022-01-04 | GSE163152 | GEO

Transcriptional profiling of platinum sensitive and platinum resistant high grade serous ovarian cancer samples

Project description:This study aims at correlating changes in the transcriptional state in high grade serous epithelial ovarian cancer (HGS-EOC) to the response to therapy, in particular the insurgence of resistance to platinum-based treatment.

2020-02-11 | E-MTAB-7083 | biostudies-arrayexpress

microRNA profiling of platinum sensitive and platinum resistant high grade serous ovarian cancer samples

Project description:This study aims at correlating changes in the microRNA state in high grade serous epithelial ovarian cancer (HGS-EOC) to the response to therapy, in particular the insurgence of resistance to platinum-based treatment.

2020-02-11 | E-MTAB-7084 | biostudies-arrayexpress

Epigenetic regulation of the homeobox gene MSX1 associates with platinum resistant disease in high grade serous epithelial ovarian cancer

Project description:Introduction: Although High Grade Serous Ovarian Cancer (HGSOC) is considered a chemo-responsive disease, a proportion of patients do not respond to platinum-based chemotherapy at presentation or have progression-free survival of <6 months. Validated biomarkers of lack of response would enable alternative treatment stratification for these patients and identify novel mechanisms of resistance. Methods: Differential DNA methylation was investigated in independent tumour sets using Illumina 27K HumanMethylation arrays and validated by bisulphite pyrosequencing. Gene expression was by Affymetrix arrays and qRT-PCR. The role of Msh homeobox 1 (MSX1) in drug sensitivity was investigated by gene reintroduction into ovarian cancer cell lines. Results: CpG sites at contiguous genomic locations within the MSX1 gene have significantly lower levels of methylation in HGSOC which recur by 6 months compared to after 12 months and/or with RECIST response (p<0.05, q<0.05). A decrease in methylation at these intragenic CpG sites was significantly correlated with decreased MSX1 gene expression. Low expression of MSX1 was associated with poor progression-free survival independent of known clinical prognostic features (p=0.014). Three mutant or wild-type TP53 expressing ovarian cancer cell lines, resistant to cisplatin, have reduced MSX1 expression compared to matched parental, platinum sensitive, lines. Re-expression of MSX1 in resistant lines led to cisplatin sensitisation, increased apoptosis, increased p21 and BAX expression. However, in two TP53-null cell lines, MSX1 failed to change cisplatin sensitivity. Conclusion: Hypomethylation of MSX1 is a biomarker of resistant HGSOC disease at presentation and identifies a novel mechanism of platinum drug resistance. Bisulphite converted DNA from the 86 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2015-11-26 | E-GEOD-75414 | biostudies-arrayexpress

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