Project description:To identify genes activated under CoCl2 treatment of a cancer cell line in an Sp1 dependent manner, we performed cDNA microarray analysis with an ovarian cancer cell line, in which Sp1 is silenced via RNA interference.
Project description:To identify genes activated under CoCl2 treatment of a cancer cell line in an Sp1 dependent manner, we performed cDNA microarray analysis with an ovarian cancer cell line, in which Sp1 is silenced via RNA interference. Cells were transfected with scramble or Sp1 siRNA and cultured for 40 h. Cells were further cultured for 4 h under 0.5 mM CoCl2 exposure. Total RNA was isolated for cDNA microarray analysis.
Project description:Identification of genes activated under CoCl2 treatment in an Sp1 dependent manner and under hypoxia without serum condition in an ovarian cancer cell line
Project description:To identify genes activated under serum starvation and hypoxia condition in an SREBP1 dependent manner, we performed cDNA microarray analysis with an ovarian cancer cell line OVSAYO.
Project description:To identify genes activated under hypoxia (1%O2) and serum-free treatment of a cancer cell line, we performed cDNA microarray analysis with an ovarian cancer cell line, OVSAYO.
Project description:To identify genes activated under hypoxia (1%O2) and serum-free treatment of a cancer cell line, we performed cDNA microarray analysis with an ovarian cancer cell line, OVSAYO. Cells were cultured under normoxia /hypoxia (1%O2) and serum-plus/serum-minus conditions for 16 hours. Total RNA was isolated for cDNA microarray analysis.
Project description:To evaluate the role of HIF1α in modulating the m6A abundance, we conducted m6A sequencing in the Kasumi-1 cell line treated with CoCl2 and echinomycin. CoCl2 can mediate the stabilization of HIF1α protein. Echinomycin is a small-molecule inhibitor of HIF1α, which functions through sequence-specific binding to HRE to competitively inhibit HIF1α binding to its target genes. The m6A sequencing results of the Kasumi-1 cell line treated with CoCl2 and non-treated control were uploaded previously (GSE168778). The differential m6A peaks analysis between CoCl2 + echinomycin group and CoCl2 group was performed.
Project description:A2780 is a cisplatin sensitive ovarian cancer cell line. A2780 ovarian cancer cells was treated with different doses of cisplatin in an attempt to identify biomarkers that can be used to predict chemoresponse. We used microarrays to identify genes induced by cisplatin in a time dependent manner.
Project description:Sp1 is a transcription factor able to regulate many genes through its DNA binding domain, containing three zinc fingers. We were interested in identifying target genes regulated by Sp1, with a special emphasis to those involved in proliferation and cancer. Our approach was to treat HeLa cells with a siRNA directed against Sp1 mRNA (siSp1) to decrease the expression of Sp1 and, in turn, the genes activated by this transcription factor. Sp1 siRNA treatment led to a great number of differentially expressed genes as determined by whole genome cDNA microarray analysis. Underexpressed genes were selected since they represent putative genes activated by Sp1. These underexpressed genes were classified in six Gene Onthology categories, namely proliferation and cancer, mRNA processing, lipidic metabolism, glucidic metabolism, transcription and translation. Putative Sp1 binding sites were found in the promoters of the selected genes using the MatchTM software. After literature mining, 11 genes were selected for further validation of their expression levels using RT-real time PCR. Underexpression was confirmed for the 11 genes plus Sp1 in HeLa cells after siSp1 treatment. Additionally, EMSA and chromatin immunoprecipitation assays were performed to test for binding between Sp1 and the promoters of these genes. We observed binding of Sp1 to the promoters of RAB20, FGF21, IHPK2, ARHGAP18, NPM3, SRSF7, CALM3, PGD and Sp1 itself. Finally, the mRNA levels of RAB20, FGF21 and IHPK2, three genes related with proliferation and cancer, were determined after overexpression of Sp1 in HeLa cells, to confirm their relationship with Sp1. The aim of our study was to evaluate, by using whole genome microarrays, the effects of a siRNA against the transcription factor of Sp1 in HeLa cells. Using this methodology genes activated by Sp1 could be downregulated. The obtective was to determine new genes regulated at the cellular level. Triplicate samples were hybridized for each experimental condition (6 samples in total). The samples provided were analyzed using the specific software GeneSpring GX.
Project description:To investigate differentially expressed lncRNAs in C2C12 myotubes with/without CoCl2 treatment, we used mouse lncRNA microarray to examine the expression of lncRNAs in C2C12 myotubes and C2C12 myotubes with CoCl2 treatment.
