RNA sequencing in ovarian cancer cell line HEYA8 in terms of ECM1 silencing and reintroduction of ECM1 subtypes ECM1a and ECM1b
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PROVIDER: PRJNA719542 | ENA |
REPOSITORIES: ENA
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Project description:Extracellular Matrix Protein-1 (ECM1) promotes tumorigenesis in multiple organs, but the mechanisms associated with the functions and putative receptors of ECM1 subtypes have yet to be systematically clarified. We found in this study that secretory ECM1a functions as an oncoprotein to induce tumorigenesis through binding of the Gly-Pro-Arg (GPR) motif to integrin aXb2 and activation of AKT/FAK/Rho/cytoskeletal signaling. Nonsecretory ECM1b binds to myosin to block myosin phosphorylation, thus preventing cytoskeletal signaling activation and tumorigenesis. Based on RNA sequencing, we further found that the heterogeneous nuclear ribonucleoprotein L-like (hnRNPLL) protein induced by ECM1a favors the alternative mRNA splicing of ECM1a to control ECM1-associated signaling and tumorigenesis. ATP binding cassette subfamily G member 1 (ABCG1) transduces ECM1a-integrin aXb2 interactive signaling to facilitate the phosphorylation of AKT/FAK/Rho/cytoskeletal molecules and to confer cisplatin resistance in cancer cells through upregulation of CD326-mediated cell stemness.
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Project description:Epithelial ovarian cancer is morphologically and clinically heterogeneous. Transcriptional profiling has revealed molecular subtypes (referred to as M-bM-^@M-^\C-signaturesM-bM-^@M-^]) that correlate to biological as well as clinical features. We aimed to determine gene expression differences between malignant, benign and borderline serous ovarian tumors, and to investigate similarities to the intrinsic molecular subtypes of breast cancer. Global gene expression profiling was performed using Illumina's HT12 Bead Arrays and applied to 59 fresh-frozen ovarian tumors. SAM analysis revealed enrichment of cell cycel processes among the malignant tumors, in line with malignant tumors being highly proliferative. The borderline tumors were split between the malignant and benign tumor clusters, indicating that borderline tumors have both malignant and benign features. Furthermore, nearest centroid classification was performed applying previously published gene profiles for the ovarian cancer C-signatures and the intrinsic breast cancer subtypes, respectively, and showed significant correlations between the malignant serous tumors and the highly aggressive C1, C2 and C4 ovarian cancer signatures, and the basal-like breast cancer subtype. The benign and borderline serous tumors together were significantly correlated to the normal-like breast cancer subtype and the ovarian cancer C3 signature. The borderline tumors, on the other hand, correlated significantly to the Luminal A breast cancer subtype. These findings remained when analyzed in a large, independent dataset. The data in this study link the transcriptional profiles of serous ovarian cancer to the intrinsic molecular subtypes of breast cancer, in line with the shared clinical and molecular features between high-grade serous ovarian cancer and basal-like breast cancer, including an aggressive phenotype, frequent TP53 mutations and a high degree of genomic instability, and suggest that biomarkers and targeted therapies may overlap between these subsets of ovarian and breast cancers. Finally, the link between benign and borderline ovarian cancer and luminal breast cancer may indicate endocrine responsiveness in a subset of ovarian cancers. Total RNA obtained from serous ovarian adenocarcinomas, adenomas and borderline tumors. Gene expression profiling using Illumina's HT12 v4 bead arrays. Application of ovarian cancer molecular subtypes and intrinsic breast cancer subtypes using nearest centroid classification. KRAS and BRAF mutation analyses in the malignant and borderline tumors.
2014-08-15 | E-GEOD-57477 | biostudies-arrayexpress
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Project description:We investigated the functions of ECM1 subtypes ECM1a (inlcuding wild type and mutant) and ECM1b in ovarian cancer cell line HEYA8. While ECM1a is oncogenic, ECM1b is a tumor suppressor. To identify the molecules binding to ECM1a or ECM1b within cells, protein samples were generated by co-IP using HA antibody to pull down proteins potentially binding to ECM1a (HA-tagged) (samples: P20170700270A1/A2/A3/A4) or ECM1b (HA-tagged) (samples: P20170700270B1/B2/B3/B4) within cells indicated in gel image P20170700270. To identify more cell surface markers besides integrins alpha X and beta 2 binding to ECM1a-WT or ECM1a-MT, three batches of protein samples were generated by co-IP using HA antibody to pull down total proteins binding to ECM1a-WT or ECM1a-MT shown in gel image R20191201880, or to pull down membrane fractionation proteins binding to ECM1a-WT or ECM1a-MT indicated in gel image 20200100053, or to pull down membrane fractionation proteins of HEYA8 cells treated with ECM1a-WT or ECM1a-MT conditioned media binding to ECM1-WT or ECM1a-MT shown in gel image 20200100054.
2021-05-27 | PXD025239 | Pride
Project description:Ovarian cancer is the most lethal gynecological malignancy. Recurrence and chemoresistance are tough challenges leading to poor prognosis. HJURP is a molecular chaperone of CENP-A, which is associated with aggressive progression in multiple tumors. However, the function of HJURP in ovarian cancer has not been elucidated. In our study, we found HJURP was over-expressed in ovarian cancer and high expression of HJURP was correlated to unfavorable prognosis. HJURP knockdown could inhibit proliferation, metastasis and induce G0/G1 stagnation of ovarian cancer cells. Besides, next-generation sequencing(NGS) unveiled that WEE1 was down-regulated by silencing HJURP. Further mechanistic research revealed that HJURP regulated WEE1 through MYC, and luciferase assay indicated that MYC was a transcription factor of WEE1. Additionally, we investigated that silencing HJURP increased sensitivity of ovarian cancer cells to cisplatin via MYC/WEE1 axis, and HJURP participated in DNA repair of cisplatin-induced damage. More interestingly, silencing HJURP could enhance sensitivity of ovarian cancer cells to AZD1775 and improve the synergistic effect of cisplatin plus AZD1775 combined therapy. Collectively, our data displays that HJURP promotes tumor progression and chemoresistance of ovarian cancer, and HJURP has potential to be a novel therapeutic target in the combined treatment with cisplatin and AZD1775 in ovarian cancer.
2022-01-26 | GSE190568 | GEO
Project description:Epithelial ovarian cancer is morphologically and clinically heterogeneous. Transcriptional profiling has revealed molecular subtypes (referred to as “C-signatures”) that correlate to biological as well as clinical features. We aimed to determine gene expression differences between malignant, benign and borderline serous ovarian tumors, and to investigate similarities to the intrinsic molecular subtypes of breast cancer. Global gene expression profiling was performed using Illumina's HT12 Bead Arrays and applied to 59 fresh-frozen ovarian tumors. SAM analysis revealed enrichment of cell cycel processes among the malignant tumors, in line with malignant tumors being highly proliferative. The borderline tumors were split between the malignant and benign tumor clusters, indicating that borderline tumors have both malignant and benign features. Furthermore, nearest centroid classification was performed applying previously published gene profiles for the ovarian cancer C-signatures and the intrinsic breast cancer subtypes, respectively, and showed significant correlations between the malignant serous tumors and the highly aggressive C1, C2 and C4 ovarian cancer signatures, and the basal-like breast cancer subtype. The benign and borderline serous tumors together were significantly correlated to the normal-like breast cancer subtype and the ovarian cancer C3 signature. The borderline tumors, on the other hand, correlated significantly to the Luminal A breast cancer subtype. These findings remained when analyzed in a large, independent dataset. The data in this study link the transcriptional profiles of serous ovarian cancer to the intrinsic molecular subtypes of breast cancer, in line with the shared clinical and molecular features between high-grade serous ovarian cancer and basal-like breast cancer, including an aggressive phenotype, frequent TP53 mutations and a high degree of genomic instability, and suggest that biomarkers and targeted therapies may overlap between these subsets of ovarian and breast cancers. Finally, the link between benign and borderline ovarian cancer and luminal breast cancer may indicate endocrine responsiveness in a subset of ovarian cancers.
2014-08-15 | GSE57477 | GEO
Project description:Background: It has been shown that based on gene expression profiles, subgroups within epithelial ovarian cancers (EOC) can be identified. We studied a well characterized series of ovarian carcinomas from patients treated at our institute using gene expression profiling to better define clinically significant subgroups. Methods: Gene expression profiling was performed using RNA of 90 primary fresh frozen EOC samples representing all histological subtypes and stages (FIGO I-IV). Patients underwent either primary or interval debulking surgery and if indicated taxane-based chemotherapy. Pathology was reviewed for all cased and complete follow-up, including treatment response and recurrences was available for all patients. Results: Unsupervised and supervised analysis of gene expression data showed distinct subtypes correlating with histology. Mucinous carcinoma was the most distinct subtype based on gene expression profile. No significant differences in gene expression profile between high and low grade serous carcinomas could be observed. No gene expression signatures associated with survival or treatment response could be identified. Conclusion: Histological subtypes of ovarian adenocarcinomas are characterized by distinct gene expression profiles. In order to find signatures correlated to outcome of treatment it is essential that gene expression profiling studies are performed in histological homogeneous groups.
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Project description:Dual Morphologic Subtypes of High-Grade Serous Ovarian Cancer
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