SK-OV-3 cells under Carboplatin
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ABSTRACT:
PROVIDER: PRJEB10024 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:SK-OV-3 cells under prolonged carboplatin exposition turn into giant cells. This dataset contains the transcriptome of cultured SK-OV-3 cells with and without carboplatin.
2016-04-30 | E-MTAB-3770 | biostudies-arrayexpress
Project description:Bone morphogenetic proteins (BMPs) are extracellular signaling molecules that belong to the transforming growth factor beta (TGF-β) superfamily. By regulating target gene transcription, BMPs control various cellular processes, such as proliferation, differentiation, apoptosis and migration. In addition, rBMP2 was used to observe BMP signaling in treatment of ovarian cancer cell line SK-OV-3. We attempted to address the possible roles of BMP signaling by inhibiting a wide-range of downstream pathways using a small molecule inhibitor of type I BMPRs, dorsomorphin. The potential utility of this molecule as a molecular inhibitor of BMP signaling in treatment of ovarian cancer cell line SK-OV-3 was also evaluated. SK-OV-3 cells were incubated in 12 separate culture dishes, 3 dishes with PBS, 3 dishes with recombinant BMP2 (rBMP2) (100 ng/ml), 3 dishes with DM (5 μM) and 3 dishes with recombinant BMP2 (rBMP2) (100 ng/ml) plus DM (5 μM) in the culture medium for 24 hours prior to the analysis.
2014-08-07 | E-GEOD-60135 | biostudies-arrayexpress
Project description:Bone morphogenetic proteins (BMPs) are extracellular signaling molecules that belong to the transforming growth factor beta (TGF-β) superfamily. By regulating target gene transcription, BMPs control various cellular processes, such as proliferation, differentiation, apoptosis and migration. In addition, rBMP2 was used to observe BMP signaling in treatment of ovarian cancer cell line SK-OV-3. We attempted to address the possible roles of BMP signaling by inhibiting a wide-range of downstream pathways using a small molecule inhibitor of type I BMPRs, dorsomorphin. The potential utility of this molecule as a molecular inhibitor of BMP signaling in treatment of ovarian cancer cell line SK-OV-3 was also evaluated.
2014-08-07 | GSE60135 | GEO
Project description:To investigate the role of PAI-1 (SERPIN E1) in ovarian cancer, we performed several in vitro assays using SK-OV-3 cells in which PAI-1 had been knocked down by siRNA, treated with platelets, or both. We then performed a comparative gene expression analysis using RNA-Seq data from untreated cells, PAI-1 siRNA knockdown or negative control, each with and without incubation with healthy donor platelets.
2023-11-29 | GSE223654 | GEO
Project description:To discover the abnormal regulatory role of Pin1 in the ovarian cancer, The Pin1 full cDNA was knockIn (KI) the normal ovarian epithelium (Hose), and parallelly Pin1 was knockdown in the Ovarian cancer cells MCAS and sk-ov-3, and then compared the expression profiles of them to discovery the key features regulated by Pin1.
2018-01-04 | GSE84539 | GEO
Project description:Gene Expression profile of xenograft tumors generated with SK-OV-3 pIND_EV (Empty vector) cells and SK-OV-3 pIND_BORA (Bora overexpressing) cells.
2022-10-22 | GSE139244 | GEO
Project description:Purpose: To investigate the expression profiles of genes regulated by bHLH6, we performed RNA-seq analysis using bHLH6 OV, spx4, and wild type treated with high and low P Methods: Roots and shoots mRNA profiles of 7-day-old bHLH6 OV, spx4, and wild-type (WT) rice seedlings treated with 200 μM or 10 μM Pi for 2 weeks three biological replicates were generated by deep sequencing using the NEBNext® UltraTM RNA Library Prep Kit for Illumina® (NEB, USA). The mapped reads of each sample were assembled by Hisat2 (v2.0.5). qRT–PCR validation was performed using SYBR Green assays Results: RNA-seq data confirmed that in shoots, 4,694 genes were upregulated and 4,126 were downregulated in bHLH6 OV lines compared with wild type under high-P conditions.Among the differentially expressed genes, 1,805 (38.5%) were upregulated in wild type under low-P conditions, whereas 1,598 (38.7%) of the downregulated genes were downregulated in wild type under low-P conditions, suggesting that bHLH6 overexpression upregulates a subset of PSI genes. In total, 971 genes were upregulated and 853 genes were downregulated in spx4 compared to wild type in high-P conditions. Among these upregulated genes, 371 (38.2%) were also upregulated in shoots of bHLH6 OV plants compared to in wild type; 456 (53.4%) of the downregulated genes were also downregulated in shoots of bHLH6 OV compared with wild type. In roots, 311 (10.5%) out of the 2,969 upregulated genes in bHLH6 OV lines under high-P conditions were also upregulated in wild type under low-P conditions; 501 (19.1%) out of the 2,628 downregulated genes in bHLH6 OV were also downregulated in wild type under low-P conditions. However, 313 (60.2%) out of the 520 genes upregulated in spx4 in roots were also upregulated in bHLH6 OV lines compared to in wild type, whereas 497 (54.6%) out of 910 the downregulated genes were also downregulated in bHLH6 OV compared to in wild type. To validate the RNA-seq results, we selected the upregulated PT and PAP (PURPLE ACID PHOSPHATASE) genes for expression analysis using RT-qPCR. The expression levels of PT2, PT10, PAP10a, and PAP21b were considerably higher in roots of bHLH6 OV plants than in those of wild type and bhlh6 mutants, whereas the expression of SPX2 was much lower in bHLH6 OV plants than in wild type Conclusion: our study is the first to analyze in detail the bHLH6 transcriptome produced by rna-seq technology and perform biological replication. Our results suggest that bHLH6 mediates the regulation of Pi homeostasis by SPX4. Our results advance the current understanding of the Pi-signaling regulatory network and will potentially contribute to the genetic improvement of crop P efficiency.
2020-12-31 | GSE147692 | GEO
Project description:Triple negative breast cancer (TNBC) is the subtype of breast cancer most lacking in efficient treatment options. Although many TNBCs show remarkable responses to carboplatin-based chemotherapy, they often develop resistance over time. With increasing use of carboplatin in clinics, there is a pressing need to understand mechanisms causing carboplatin resistance and identify the vulnerabilities of carboplatin-resistant tumors. We generated carboplatin-resistance models based on the TNBC cell line MDA-MB-468 and patient derived xenograft (PDX) models of TNBCs. By combining the results of mass spectrometry-based proteome profiling and a kinome RNA interference screen, we assessed the molecular changes and vulnerabilities of carboplatin-resistant TNBCs. Using pharmacological inhibition of the identified targets, we validated the dependencies of carboplatin-resistant cells in vitro and in PDX models. We found that carboplatin resistance in TNBC is accompanied by drastic proteome rewiring. Carboplatin-induced metabolism alterations and upregulation of anti-oxidative response keep low levels of DNA damage and support cell replication in the presence of carboplatin. Carboplatin-resistant cells also exhibited longer mitosis due to dysregulation of mitotic checkpoint. Whereas the components of the mitotic checkpoints, AURKA and BUB1, are essential for the viability of carboplatin-resistant cells, the checkpoint kinases CHEK1 and WEE1 are indispensable for survival of carboplatin-treated resistant cells. We confirmed that pharmacological inhibition of CHEK1 by prexasertib in the presence of carboplatin is well tolerated by mice and suppresses the growth of carboplatin-resistant TNBC xenografts. Abrogation of the mitotic checkpoint re-sensitizes carboplatin-resistant TNBCs to carboplatin. CHEK1 inhibition represents a potential strategy for the treatment of carboplatin-resistant TNBCs.
2021-07-07 | PXD021726 | Pride
Project description:Following the re-exposure to lipopolysaccharide (LPS), macrophages exhibit the immunosuppressive state contribute to low production of proinflammatory cytokines and inability to respond the stimuli, a phenomenon is termed “tolerance”. Histone modification has been found in LPS-induced tolerant macrophages. Carboplatin, an antitumor drug, exerts its general effect on inhibition of DNA replication and transcription as well as epigenetic modification. Therefore, we hypothesized that carboplatin can be used to rescue the tolerance in macrophages. We found that carboplatin increases IL-6 but not TNF-α production in LPS-primed cells. The significant inductions were examined in carboplatin-treated tolerant macrophages evaluated by ELISA and qPCR. GSEA analyses revealed that p53 was the significant hallmark in both primed and tolerant RNA-Seq transcripts under carboplatin exposure while E2F ang G2/M were the upmost in negative hallmarks. HP1-α, heterochromatin protein 1, was significantly reduced in carboplatin-treated tolerant macrophages. The significant lower transcript of H3K9me3 methyltransferase, setdb2, was determined whereas kdm4d, demethylase encoding gene was significantly up-regulated in the presence of carboplatin in tolerant macrophages. Based on our data we suggested that carboplatin mediated upregulation of proinflammatory cytokine and rescue tolerance via the H3K9me3 modification. Carboplatin is potentially be a therapeutic drug for tolerance recovery in sepsis patients.
2021-11-10 | GSE179974 | GEO