Effect of therapy-induced secretomes on the transcriptome of ovarian cancer cells
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ABSTRACT:
PROVIDER: PRJNA1010741 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25796783_1.fastq.gz | Fastqsanger.gz | |||
| SRR25796783_2.fastq.gz | Fastqsanger.gz | |||
| SRR25796784_1.fastq.gz | Fastqsanger.gz | |||
| SRR25796784_2.fastq.gz | Fastqsanger.gz | |||
| SRR25796785_1.fastq.gz | Fastqsanger.gz |
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Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. Recently, we examined how cancer cell secretome changes in response to chemotherapy. We showed that tumor therapy-induced secretomes significantly increased resistance of cancer cells to subsequent cisplatin treatment but we did not observed the same phenomenon on normal fibroblasts. To elucidate how therapy-induced secretomes affect the transcriptomic profiles of recipient tumor cells, we incubated SKOV3 cells for 3 days with secretomes from control or dying cancer cells. The same conditions were used for normal fibroblasts. Enrichment analysis of differentially expressed genes in SKOV3 cells incubated with therapy-induced secretomes identified prominent up-regulation of genes involved in coordination of mitotic processes, G2/M transition checkpoints and DNA repair. These findings demonstrate that under stress condition cancer but not normal cells can secrete signaling molecules into the exracellular space and contribute to the emergence of tumor chemoresistance during short time period.
2024-04-24 | GSE241910 | GEO
Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. Recently, we examined how cancer cell secretome changes in response to chemotherapy. Moreover, therapy-induced secretomes significantly increased resistance of cancer cells to subsequent cisplatin treatment. To elucidate how therapy-induced secretomes affect the proteomic profiles of recipient tumor cells, we incubated SKOV3 cells for 3 days with secretomes from control or dying cancer cells. Enrichment analysis of differentially abundant proteins revealed that therapy-induced secretomes provoked increase abundance of proteins involved in DNA repair and cell cycle regulation. These findings demonstrate that under stress condition cancer cells can secrete signaling molecules into the extracellular space and contribute to the emergence of tumor chemoresistance during short time period.
2024-05-29 | PXD027794 | Pride
Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. To identify extracellular signaling molecules that potentially contribute to the development of therapy resistance, we examined how cancer cell secretome changes in response to chemotherapy. We performed LC-MS/MS analysis of secretomes from several ovarian cancer cell lines representing different tumor subtypes: serous ovarian cancer cell line (OVCAR3), ovarian cystadenocarcinoma cell line (MESOV) and clear cell ovarian cancer primary culture isolated from ascites (cells 26) before and 48 hours after cisplatin treatment. In addition, we studied secretomes from keratinocyte-derived epithelial cell line HaCaT as non-cancerous “normal” cells. Functional annotation of proteins which secretion increased after cisplatin showed that these proteins were mainly associated with cluster of spliceosome.
2024-05-29 | PXD045663 | Pride
Project description:Ovarian cancer is characterized by transcoelomic metastasis into the peritoneal cavity. The peritoneal malignant ascites is enriched with ovarian cancer cells and a small amount of tumor-associated immune cells which create a unique microenvironment actively contributing to progression of the disease. However, it remains unclear how cancer cells communicate to its local environment under the influence of chemotherapy. To address this issue, we performed LC-MS/MS analyses of several primary cultures of ovarian cancer cells from chemonaive malignant ascites incubated for 3 days with autologous pre- or post-chemotherapy ascitic fluids. Enrichment analysis identified prominent upregulation of proteins associated with pathways of DNA repair and cell cycle regulation in tumor cells incubated with ascitic fluids after chemotherapy. Consistently with these data, ascites after therapy increased the resistance of ovarian cancer cells to cisplatin. These findings demonstrate that under stress condition cancer cells can secrete signaling molecules into the extracellular space and contribute to the emergence of tumor chemoresistance during short time period.
2024-05-29 | PXD045647 | Pride
Project description:We showed that in response to chemotherapy, dying cancer cells can secrete spliceosomal components into the extracellular space. These therapy-induced secretomes enriched with spliceosomal components promote the chemoresistance of recipient tumor cells. We demonstrated that spliceosomal proteins SNU13 and SYNCRIP can relocalize from dying tumor cells to recipient tumor cells via extracellular vesicles. To investigate whether the increased abundance of splicing factors could be the reason for the acquisition of a more aggressive phenotype by tumor cells, we got SKOV3 cell lines stably overexpressing SYNCRIP or SNU13. These cell lines were more resistant to cisplatin compared to control cell line expressing empty vector. Next, to investigate how the therapy response is formed in tumor cells with and without overexpression of spliceosomal proteins SNU13 or SYNCRIP, we performed RNAseq analysis of these cells before and 24 hours after cisplatin treatment. Enrichement analyses showed that in response to cisplatin, genes associated with DNA repair and cell cycle regulation were upregulated in cancer cell lines overexpressing SYNCRIP or SNU13 compared with control cells. This study revealed previously unknown signaling molecules in the microenvironment of ovarian cancer that have potential clinical significance.
2024-04-24 | GSE241913 | GEO
Project description:Exogenous signals from drug-stressed cancer cells promote acquisition of a more aggressive phenotype of neighboring tumor cells. To identify extracellular signaling molecules that potentially contribute to the development of therapy resistance, we examined how cancer cell secretome changes in response to chemotherapy. We performed LC-MS/MS analysis of conditioned media (CM) from ovarian cancer cells SKOV3 before and 48 hours after cisplatin treatment. We identified 1,820 and 784 proteins in secretomes of cancer cells treated or untreated with cisplatin, respectively. Functional annotation of proteins which secretion increased after cisplatin showed that these proteins were mainly associated with cluster of spliceosome. To investigate whether secretion of spliceosomal proteins during induction of apoptosis is a specific property of tumor cells, we compared proteomes of CM from primary culture of normal human skin fibroblasts before and 48 hours after exposure to cisplatin (IC50). A LC-MS/MS analysis revealed that most of the proteins in the CM of fibroblasts and cancer cells under normal conditions overlap, while the secretomes after therapy demonstrate much more pronounced differences. GO and KEGG enrichment analysis revealed higher abundance of cell adhesion and extracellular matrix proteins in CM of fibroblasts before chemotherapy; while lysosomal proteins and growth factors, associated with wound healing were increased after cisplatin treatment. Spliceosomal proteins were only slightly present in fibroblast CM and did not show any changes in a response to chemotherapy. We suggest that the acquisition of ovarian cancer chemoresistance might be partially mediated by extracellular spliceosomal components.
2024-05-29 | PXD019096 | Pride
Project description:Therapy-induced Secretion of Spliceosomal Components Mediates Pro-Survival Crosstalk Between Ovarian Cancer Cells
| PRJNA1010733 | ENA
Project description:Essential role of PLD2 in hypoxia-induced stemness and therapy resistance in ovarian tumors
| PRJNA866399 | ENA
Project description:The purpose of this study was to characterise the effects of trastuzumab and pertuzumab, either as single agents or as combination therapy on gene and protein expression in human ovarian cancer in vivo. Illumina BeadChips were used to profile the transcriptome after four days treatment of SKOV3 tumor xenografts. Although genes involved with HER2, MAP-kinase and p53 signaling pathways were commonly induced by all treatments, a greater number and variety of genes were differentially expressed by the complementary combination therapies compared to either drug on its own. The protein level of the CDK-inhibitors p21 and p27 were increased in response to both agents alone and further by the combination; pERK signaling was inhibited by all treatments; but only pertuzumab alone inhibited pAkt signaling. The expression of proliferation, apoptosis, cell division and cell cycle markers was distinct in a panel of primary ovarian cancer xenografts, suggesting heterogeneity of response in ovarian cancer and the need to establish biomarkers of response. This first comprehensive study of the molecular response to trastuzumab, pertuzumab and combination therapy in vivo highlights that there are both common and distinct downstream effects to different HER2 antibodies and that pathways may be invoked more strongly or in a different manner by a combination of agents. Some of the in vivo results for ovarian tumors differ from previous in vitro studies in breast cancer cells, emphasizing that the molecular response to anti-cancer agents involves variable and complex disease-specific interactions of signaling mechanisms. SCOV3 Ovarian cell line xenografts treated with Trastuzumab, pertuzumab or combination after 4 days
2012-05-02 | E-GEOD-31432 | biostudies-arrayexpress