RNA sequencing of RRM2 overexpressing in PC-3 cells
Ontology highlight
ABSTRACT: Human prostate cancer PC-3 cells stably overexpress RRM2. Overexpression of RRM2 were confirm by westernblot or qPCR. Transfected cells were prepared for RNA-seq.
Project description:Human prostate cancer LNCaP cells stably overexpress RRM2. Overexpression of RRM2 were confirm by westernblot or qPCR. Transfected cells were prepared for RNA-seq.
Project description:Human prostate cancer C4-2 cells transfected with siRNAs (siNS and siRRM2). Knockdown were confirm by westernblot or qPCR. Transfected cells were prepared for RNA-seq.
Project description:PC-3 cells stably transfected with PIM1 overexpressing vector and transiently transfected with wt or multi-mutant NFATC1 overexpressing vector
Project description:A proteomic comparison between normal HT-1080 cells and HT-1080 cells that have been stably transfected to overexpress protein arginie and glutamate rich 1 (ARGLU1).
Project description:The 22Rv1 and PC-3 cells were transduced with shMIMIC human lentiviral vectors (Horizon Discovery, Cambridge, UK) to stably overexpress miRNA-23c or -4328. The SMARTvector Non-Targeting Control (NTC) was expressed to serve as a negative control. The vectors contained a turbo green fluorescent protein (turboGFP) and a puromycin resistance gene cassette. After transduction, cells were cultured in a medium supplemented with 5 µg/mL puromycin (Takara Bio, Tokyo, Japan) for antibiotic selection. Overexpression was confirmed by monitoring the turboGFP by fluorescence microscopy and by RT-qPCR analysis of miRNA-23c and -4328 levels. Relative protein quantification was performed to compare protein expression in 22Rv1 and PC-3 single cell clones overexpressing miRNA-23c and -4328, compared to corresponding NTC cells. Single cell clones overexpressing either miRNA-23c (n = 3), -4328 (n = 3) or NTC (n = 3) were analyzed in triplicate.
Project description:We previously demonstrated that the osteopontin-c (OPNc) splice variant activates several aspects of the progression of prostate cancers. The goal of the present study was to develop cell line model to determine the impact of OPNc overexpression on main cancer signaling pathways and thus obtain insights into the mechanisms of OPNc pro-tumorigenic roles. Methods: PC-3 cells were stably transfected to overexpress OPNc. Transcriptomic profiling was performed on these cells and compared to controls, to identify OPNc overexpression-dependent changes in gene expression levels and pathways by qRT-PCR analyses; Results: Of 84 genes tested by using a multiplex real-time PCR Cancer Pathway Array approach, among then 16 were differentially expressed between PC-3 OPNc-overexpressing cells in relation to control clones. Differentially expressed genes are included in all main hallmarks of cancer, and several interacting proteins have been identified using an interactome network analysis. Conclusions: Overall, the present study elucidated transcriptional changes of prostate cancer cells in response to OPNc overexpression, which provides an assessment for predicting the molecular mechanisms by which this splice variant promotes tumor progression features.
Project description:Transcriptional profiling of the prostate adenocarcinoma cell line PC-3 comparing control cells transfected with a pool of oligonucleotides control (siControl) with cells transfected a pool of oligonucleotides specific to inhibit ARHGAP21 expression (siARHGAP21). The efficiency of the transfection was checked with quantitative PCR and western blotting. Goal was to determine the effects of ARHGAP21 silencing on global PC-3 gene expression.