Transcriptome profiling of taxane-resistant, castration-resistant prostate cancer cells versus parental control cells
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ABSTRACT:
PROVIDER: PRJNA707219 | ENA |
REPOSITORIES: ENA
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Project description:The purpose of the study was to assess the transcriptomic differences between taxane-resistant cell lines and parental control cells to identify drivers of resistance.
2021-08-22 | GSE168397 | GEO
Project description:We sought to compare mRNA expression profiles between the parental SKOV3ip1 and taxane-resistant SKOV3TRip2 in order to determine what genes are mediating taxane resistance
2011-01-01 | GSE23779 | GEO
Project description:Taxane resistant breast cancer cells
| PRJEB13235 | ENA
Project description:We sought to compare mRNA expression profiles between the parental SKOV3ip1 and taxane-resistant SKOV3TRip2 in order to determine what genes are mediating taxane resistance 3 separate collections of each cell line were made, with cells at 75-80% confluence growing on 2-dimentional culture plates, and RNA extracted with RNAeasy kit Authors were unable to retrieve raw data.
2011-01-01 | E-GEOD-23779 | biostudies-arrayexpress
Project description:Background: The acquisition of drug resistance is one of the most malignant phenotypes of cancer. MicroRNAs (miRNAs) have been implicated in various types of cancers, but its role in taxane-resistance of prostate cancer remains poorly understood. Methods: In order to identify miRNAs related to taxane-resistance, miRNA profiling was performed using prostate cancer PC3 cells and paclitaxel-resistant PC3 cell lines established from PC3 cells. Microarray analysis of mRNA expression was also conducted to search for potential target genes of miRNA. The effects of ectopic expression of miRNA on cell growth, tubulin polymerization, drug sensitivity and apoptotic signaling pathway were investigated in a paclitaxel-resistant PC3 cell line. Results: The expression of miR-130a was down-regulated in all paclitaxel-resistant cell lines compared with parental PC3 cells. Based on mRNA microarray analysis, we identified SLAIN1 and CAV2 as potential target genes for miR-130a. Transfection with a miR-130a precursor into a paclitaxel-resistant cell line suppressed cell growth and increased the sensitivity to paclitaxel. Lastly, ectopic expression of miR-130a did not affect the polymerized tubulin level, but activated apoptotic signaling through activation of caspase-8. Conclusion: These results suggested that miR-130a may be involved in the paclitaxel-resistance and could be a therapeutic target for taxane-resistant prostate cancer.
2015-07-31 | GSE64013 | GEO
Project description:Background: The acquisition of drug resistance is one of the most malignant phenotypes of cancer. MicroRNAs (miRNAs) have been implicated in various types of cancers, but its role in taxane-resistance of prostate cancer remains poorly understood. Methods: In order to identify miRNAs related to taxane-resistance, miRNA profiling was performed using prostate cancer PC3 cells and paclitaxel-resistant PC3 cell lines established from PC3 cells. Microarray analysis of mRNA expression was also conducted to search for potential target genes of miRNA. The effects of ectopic expression of miRNA on cell growth, tubulin polymerization, drug sensitivity and apoptotic signaling pathway were investigated in a paclitaxel-resistant PC3 cell line. Results: The expression of miR-130a was down-regulated in all paclitaxel-resistant cell lines compared with parental PC3 cells. Based on mRNA microarray analysis, we identified SLAIN1 and CAV2 as potential target genes for miR-130a. Transfection with a miR-130a precursor into a paclitaxel-resistant cell line suppressed cell growth and increased the sensitivity to paclitaxel. Lastly, ectopic expression of miR-130a did not affect the polymerized tubulin level, but activated apoptotic signaling through activation of caspase-8. Conclusion: These results suggested that miR-130a may be involved in the paclitaxel-resistance and could be a therapeutic target for taxane-resistant prostate cancer.
2015-07-31 | GSE64012 | GEO
Project description:Background: The acquisition of drug resistance is one of the most malignant phenotypes of cancer. MicroRNAs (miRNAs) have been implicated in various types of cancers, but its role in taxane-resistance of prostate cancer remains poorly understood. Methods: In order to identify miRNAs related to taxane-resistance, miRNA profiling was performed using prostate cancer PC3 cells and paclitaxel-resistant PC3 cell lines established from PC3 cells. Microarray analysis of mRNA expression was also conducted to search for potential target genes of miRNA. The effects of ectopic expression of miRNA on cell growth, tubulin polymerization, drug sensitivity and apoptotic signaling pathway were investigated in a paclitaxel-resistant PC3 cell line. Results: The expression of miR-130a was down-regulated in all paclitaxel-resistant cell lines compared with parental PC3 cells. Based on mRNA microarray analysis, we identified SLAIN1 and CAV2 as potential target genes for miR-130a. Transfection with a miR-130a precursor into a paclitaxel-resistant cell line suppressed cell growth and increased the sensitivity to paclitaxel. Lastly, ectopic expression of miR-130a did not affect the polymerized tubulin level, but activated apoptotic signaling through activation of caspase-8. Conclusion: These results suggested that miR-130a may be involved in the paclitaxel-resistance and could be a therapeutic target for taxane-resistant prostate cancer. Human hormone-refractory prostate cancer PC3 cells were cultured in RPMI1640 medium supplemented with 10 % of fetal bovine serum, 100 units/ml of penicillin and 100 ug/ml of streptomycin. Paclitaxel-resistant PC3PR20, PC3PR70 and PC3PR200 cells, which respectively could proliferate in the presence of 20, 70 and 200 nM of paclitaxel (Sigma-Aldrich, St. Louis, MO, USA), were previously established from PC3 cells by a stepwise increase of paclitaxel in the culture medium (Kojima et al, 2010, Prostate 70: 1501-12).
2015-07-31 | E-GEOD-64013 | biostudies-arrayexpress
Project description:While taxane-platin standard chemotherapy provides benefit in advanced and localized non-small cell lung cancer (NSCLC), the majority of patients relapse with drug resistant tumors. Mechanisms underlying NSCLC resistance to this standard doublet chemotherapy are still not fully understood, and treatment options for chemoresistant lung tumors are limited. The goals of this work were to establish new preclinical NSCLC models of resistance to taxane-platin doublet chemotherapy, identify mechanisms of resistance, and develop new rational pharmacologic approaches to target drug resistant NSCLCs.
2016-12-31 | GSE77209 | GEO
Project description:Background: The acquisition of drug resistance is one of the most malignant phenotypes of cancer. MicroRNAs (miRNAs) have been implicated in various types of cancers, but its role in taxane-resistance of prostate cancer remains poorly understood. Methods: In order to identify miRNAs related to taxane-resistance, miRNA profiling was performed using prostate cancer PC3 cells and paclitaxel-resistant PC3 cell lines established from PC3 cells. Microarray analysis of mRNA expression was also conducted to search for potential target genes of miRNA. The effects of ectopic expression of miRNA on cell growth, tubulin polymerization, drug sensitivity and apoptotic signaling pathway were investigated in a paclitaxel-resistant PC3 cell line. Results: The expression of miR-130a was down-regulated in all paclitaxel-resistant cell lines compared with parental PC3 cells. Based on mRNA microarray analysis, we identified SLAIN1 and CAV2 as potential target genes for miR-130a. Transfection with a miR-130a precursor into a paclitaxel-resistant cell line suppressed cell growth and increased the sensitivity to paclitaxel. Lastly, ectopic expression of miR-130a did not affect the polymerized tubulin level, but activated apoptotic signaling through activation of caspase-8. Conclusion: These results suggested that miR-130a may be involved in the paclitaxel-resistance and could be a therapeutic target for taxane-resistant prostate cancer. Human hormone-refractory prostate cancer PC3 cells were cultured in RPMI1640 medium supplemented with 10 % of fetal bovine serum, 100 units/ml of penicillin and 100 ug/ml of streptomycin. Paclitaxel-resistant PC3PR20, PC3PR70 and PC3PR200 cells, which respectively could proliferate in the presence of 20, 70 and 200 nM of paclitaxel (Sigma-Aldrich, St. Louis, MO, USA), were previously established from PC3 cells by a stepwise increase of paclitaxel in the culture medium (Kojima et al, 2010, Prostate 70: 1501-12).
2015-07-31 | E-GEOD-64012 | biostudies-arrayexpress
Project description:The development of taxane resistance remains a major challenge for castration resistant prostate cancer (CR-PCa), despite the effectiveness of taxanes in prolonging patient survival. To uncover novel targets, we performed an epigenetic drug screen on taxane (docetaxel and cabazitaxel) resistant CR-PCa cells. We identified BRPF reader proteins, along with several epigenetic groups (CBP/p300, Menin-MLL, PRMT5 and SIRT1) that act as targets effectively reversing the resistance mediated by ABCB1. Targeting BRPFs specifically resulted in the resensitization of resistant cells, while no such effect was observed on the sensitive compartment. These cells were successfully arrested at the G2/M phase of cell cycle and underwent apoptosis upon BRPF inhibition, confirming the restoration of taxane susceptibility. Pharmacological inhibition of BRPFs reduced ABCB1 activity, indicating that BRPFs may be involved in an efflux-related mechanism. Indeed, ChIP-qPCR analysis confirmed binding of BRPF1 to the ABCB1 promoter suggesting direct regulation of the ABCB1 gene at the transcriptional level. RNA-seq analysis revealed that BRPF1 knockdown affects the genes enriched in mTORC1 and UPR signaling pathways, revealing potential mechanisms underlying its functional impact, which is further supported by the enhancement of taxane response through the combined inhibition of ABCB1 and mTOR pathways, providing evidence for the involvement of multiple BRPF1-regulated pathways. Beyond clinical attributes (Gleason score, tumor stage, therapy outcome, recurrence), metastatic PCa databases further supported the significance of BRPF1 in taxane resistance, as evidenced by its upregulation in taxane-exposed PCa patients.
2023-11-17 | GSE247557 | GEO