Ontology highlight
ABSTRACT:
PROVIDER: PRJNA120175 | ENA |
REPOSITORIES: ENA
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Project description:The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors. Total RNA extraction and hybridization on Affymetrix microarrays of rapamycin sensitive (RS) cells (BC3H1, mouse brain tumor cell line with myogenic properties, ATCC) cultured in Dulbecco’s modified essential medium (DMEM) media supplemented with 20% fetal bovine serum (FBS), penicillin (100 U/ml) and streptomycin (100 mg/ml). Rapamycin resistant cells (RR1) were developed by culturing BC3H1 cells in the presence of 1 uM rapamycin for 6 months. Three samples in triplicates: 1) Rapamycin sensitive cells treated with DMSO for 24 h(BC3H1, reference), 2) Rapamycin sensitive cells treated for 24 h with 100 nM rapamycin (BC3H1+R), 3) Rapamycin resistant cells constantly treated with 1uM Rapamycion (RR1+R).
2013-02-08 | E-GEOD-19885 | biostudies-arrayexpress
Project description:MicroRNAs mediate rapamycin resistance in a myogenic tumor cell line
| PRJNA123697 | ENA
Project description:The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors. Total RNA was extracted from rapamycin sensitive (RS) cells (BC3H1, mouse brain tumor cell line with myogenic properties, ATCC) cultured in Dulbecco’s modified essential medium (DMEM) media supplemented with 20% fetal bovine serum (FBS), penicillin (100 U/ml) and streptomycin (100 mg/ml). Rapamycin resistant cells (RR1) were developed by culturing BC3H1 cells in the presence of 1 uM rapamycin for 6 months. Three samples in quadruplicate 1)RS cells treated with DMSO for 24 h(BC3H1, reference), 2) RS cells treated for 24 h with 100 nM rapamycin (BC3H1+R), 3) RR1 cells consantly treated with 1uM Rapamycion (RR1+R). For each experiment, 1 μM of total RNA was labeled with Hy3TM dye and a reference RNA pool (consisting of a mixture of equal amounts of total RNA from BC3H1, BC3H1+R and RR1+R cells) was labeled with Hy5TM dye using the miRCURYTM Labeling Kit. The samples were hybridized to Exiqon miRCURYTM LNA Arrays (V10.0).
2013-02-08 | E-GEOD-19916 | biostudies-arrayexpress
Project description:The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors.
2013-02-08 | GSE19916 | GEO
Project description:The mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation. Inhibitors of mTOR are being evaluated as anti-tumor agents. Given the emerging role of microRNAs (miRNAs) in tumorgenesis we hypothesized that miRNAs could play important roles in the response of tumors to mTOR inhibitors. Rapamycin resistant myogenic cells developed by long-term rapamycin treatment showed extensive reprogramming of miRNAs expression, characterized by up-regulation of the mir-17~92 and related clusters and down-regulation of tumor-suppressor miRNAs. Antagonists of oncogenic miRNA families and mimics of tumor suppressor miRNAs (let-7) restored rapamycin sensitivity in resistant tumor cells. This study identified miRNAs as new downstream components of the mTOR-signaling pathway, which may determine the response of tumors to mTOR inhibitors.
2013-02-08 | GSE19885 | GEO
Project description:Two rat hepatic cell lines, WB-F344 and WB311, were characterized for the effect of rapamycin on gene expression. The WB311 cell line, which is tumorigenic and resistant to the growth inhibitory effects of rapamycin, was originally derived from the WB-F344 parental hepatic epithelial cell line. The goal of this experiment was to identify genes that responded to rapamycin in the sensitive cells but not the resistant cells, thereby providing insight into the mechanism of rapamycin resistance.
2009-09-20 | GSE17661 | GEO
Project description:Two rat hepatic cell lines, WB-F344 and WB311, were characterized for the effect of rapamycin on gene expression. The WB311 cell line, which is tumorigenic and resistant to the growth inhibitory effects of rapamycin, was originally derived from the WB-F344 parental hepatic epithelial cell line. The goal of this experiment was to identify genes that responded to rapamycin in the sensitive cells but not the resistant cells, thereby providing insight into the mechanism of rapamycin resistance. Experiment Overall Design: Total RNA for each of four experimental groups was prepared and analyzed in triplicate: WB-F344, vehicle control; WB-F344, rapamycin; WB311, vehicle control; WB311, rapamycin.
2009-09-25 | E-GEOD-17661 | biostudies-arrayexpress
Project description:Gene expression data from rapamycin resistant and sensitive cell lines
| PRJNA123699 | ENA
Project description:The development of drug resistance is still a major impediment for the successful treatment of cancer, such as advanced stage ovarian cancer, which has a 5-year survival rate of only 30%. The molecular processes that contribute to resistance have been extensively studied, however, not much is known about the role of microRNAs. We compared microRNA expression profiles of three isogenic cisplatin sensitive and resistant cell line pairs. The only microRNA that was consistently downregulated (FDR = 0.000) in all resistant cell lines was miR-634. We investigated the effects of miR-634 modulation in ovarian cancer cell lines and patient derived tumor cells. Overexpression of miR-634 gave rise to a modest G1 phase block and enhanced apoptosis. Furthermore, miR-634 resensitized resistant ovarian cancer cell lines and patient derived tumor cells to cisplatin chemotherapy. Similarly, miR-634 enhanced the response of tumor cells to carboplatin and doxorubicin, but not to paclitaxel. We showed that miR-634 regulates cyclin D1 (CCND1), which is required for the G1-S phase transition, explaining the effects on the cell cycle. In addition, miR-634 repressed expression of GRB2, ERK2, RSK1 and RSK2, components of the Ras-MAPK pathway. Altogether, our findings suggest that miR-634 modulates several cancer relevant targets and therefore miR-634 is an attractive therapeutic candidate to resensitize chemotherapy resistant ovarian tumors. The miRNA expression profile was determined of three cisplatin sensitive/resistant cell line pairs (ovarian cancer cell line pair A2780/A2780 DDP; colon cancer cell line pair HCT8/HCT8 DDP; bladder cancer cell line pairT24/T24 DDP10).
2014-02-04 | E-GEOD-54665 | biostudies-arrayexpress
Project description:Gene expression profiles were assessed for vincristine-sensitive parental ovarian tumor cell line (SKOV3) and its highly vincristine-resistant derivative (SKVCR 2.0) Keywords: vincristine, drug resistance, ovarian, SKOV3, MDR
2007-08-24 | GSE7556 | GEO