Project description:SK-MEL-2 cells treated with Ad-E2F-1 (MOI 2), Ad-E2F-1 (MOI 2)plus doxorubicin 0.1uM, or Ad-LacZ (MOI 2) plus doxorubicin 0.1uM. The combination of E2F-1 gene therapy and chemotherapy produces a synergistic effect on melanoma cell apoptosis. However, the molecular mechanisms have not been fully elucidated. The purpose of this study was to identify novel genes or pathways that may play key roles in apoptosis when E2F-1 gene therapy is combined with doxorubicin chemotherapy. MATERIALS AND METHODS: SK-MEL-2 melanoma cells were infected with Ad-E2F-1 alone, Ad-E2F-1 plus doxorubicin, or Ad-LacZ plus doxorubicin. After 16 hours of treatment, the total RNA was extracted from these cells and subjected to microarray analysis. Quantitative real-time PCR was performed to confirm the microarray data. RESULTS: Our results showed that the combination treatment of Ad-E2F-1 and doxorubicin affected the expression of cytokines, transcription factors, as well as genes involved in signal transduction, cell cycle regulation and apoptosis. CONCLUSION: Our findings have identified, for the first time, novel molecular targets and pathways that led to apoptosis in melanoma cells when Ad-E2F-1 was combined with doxorubicin. The molecular information provided here will enhance further mechanistic studies.
Project description:Analysis of the H3K9me3 and H4K20me3 differential localization over the genome of cancer cells in three conditions: proliferating cells, doxorubicin-treated cells (senescent) and INK128-treated cells (diapause-like). Two cell lines were used to perform the experiment: human melanoma SK-mel-147 cells and human NSCLC A549 cells.
Project description:RNA-sequencing of senescent (doxorubicin) human melanoma SK-MEL-103 cells and human fetal lung fibroblast IMR-90 with different interventions
Project description:RNA-sequencing of proliferating, doxorubicin-induced senescent, palbociclib (CDK4/6i)-induced senescent and INK128-induced diapause-like human melanoma SK-MEL-147 cells and human NSCLC A549
Project description:Transcriptional profiling of the melanoma SK-mel-103 comparing control untreated cells with cells treated with 1ug/ml of polyinosine-polycytidylic acid (pIC) or 1ug/ml of pIC with polyethyleneimine (PEI) for 4 or 10 hours. Keywords: Treatment Four-condition experiment, SK-Mel-103 untreated vs. SK-Mel-103 treated with pIC/pIC+PEI at 4 and 10 hours. One replicate per array.
Project description:Analysis of transcriptome kinetics of SW1736 thyroid cancer cell line vs SK-MEL-28 melanoma cell line at various times after addition of 2 µM vemurafenib. The hypothesis tested was that SW1736 cells (vemurafenib-refractory) differentially express genes compared to SK-MEL-28 cells (vemurafenib sensitive) that confer resistance to the RAF inhibitor. Total RNA was obtained from lysates of SW1726 and SK-MEL-28 cells treated with 2 µM vemurafenib for 0, 1, 6 and 48 h. Experiment was made by triplicate.
Project description:Analysis of varied biologic pathways in neuroblastoma SK-N-SH cells grown in doxorubicin and/or SAHA. The hypothesis was that SK-N-SH cells undergo a mesenchymal change through mesenchymal change resulting in a more invasive as well as drug resistant phenotype, and that the mechanism of SAHAs effect on drug resistance may be revealed through this analysis. Total RNA was isolated from wild type, SAHA treated wild type cells, doxorubicin resistant, and SAHA treated doxorubicin resistant SK-N-SH cell lines in triplicate.
Project description:Analysis of varied biologic pathways in neuroblastoma SK-N-Be(2)C cells grown in doxorubicin and/or SAHA. We hypothesized that SK-N-Be(2)C cells undergo a mesenchymal change through mesenchymal change resulting in a more invasive as well as drug resistant phenotype, and that the mechanism of SAHAs effect on drug resistance may be revealed through this analysis. Total RNA was isolated from wild type, SAHA treated wild type cells, doxorubicin resistant, and SAHA treated doxorubicin resistant SK-N-Be(2)C cell lines in triplicate.
