Transcription profiling of different human melanoma cells in response to 5-aza-deoxycytidine
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Halaban R
PROVIDER: S-ECPF-MTAB-185 | biostudies-other | 2009
REPOSITORIES: biostudies-other
Similar Datasets
Project description:(subset of yale_halaban_skinspore_1) expression analysis in response to 5-aza-deoxycytidine and normal melanocytes versus melanoma.
2010-01-18 | E-MTAB-185 | biostudies-arrayexpress
Project description:Malignant melanoma is a common and frequently lethal disease. Current therapeutic interventions have little effect on survival, emphasizing the need for a better understanding of the genetic, epigenetic, and phenotypic changes in melanoma formation and progression. We identified genes that were not previously known to be silenced by methylation in melanoma using a microarray-based screen following treatment of melanoma cell lines with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine. Experiment Overall Design: RNA was isolated following 0 and 48 hours of 5AzadC treatment of melanocytes and six melanoma cell lines (MelJuSo, UACC 903, C8161, Neo6 C8161, WM1205, and WM35) and used for the reexpression microarray analysis.
| S-ECPF-GEOD-9118 | biostudies-other
Project description:Background: UV exposure-induced oxidative stress is implicated as a driving mechanism for melanoma. Increased oxidative stress results in DNA damage and epigenetic dysregulation. Accordingly, we explored whether a low dose of the antioxidant sulforaphane (SFN) in combination with the epigenetic drug 5-aza-2'-deoxycytidine (DAC) could slow melanoma cell growth. SFN is a natural bioactivated product of the cruciferous family, while DAC is a DNA methyltransferase inhibitor. Methods: Melanoma cell growth characteristics, gene transcription profiles, and histone epigenetic modifications were measured after single and combination treatments with SFN and DAC. Results: We detected melanoma cell growth inhibition and specific changes in gene expression profiles upon combinational treatments with SFN and DAC, while no significant alterations in histone epigenetic modifications were observed. Dysregulated gene transcription of a key immunoregulator cytokine-C-C motif ligand 5 (CCL-5)-was validated. Conclusions: These results indicate a potential combinatorial effect of a dietary antioxidant and an FDA-approved epigenetic drug in controlling melanoma cell growth.
| S-EPMC6789461 | biostudies-literature
Project description:BACKGROUND:Most patients with advanced Ewing's sarcoma (EWS) respond poorly to conventional chemotherapy, indicating the need for new treatment approaches. Epigenetic events, such as promoter hypermethylation and chromatin histone deacetylation, silence the expression of tumor suppressor genes (TSGs) and play an important role in tumorigenesis. These epigenetic changes can be reversed by using 5-aza-2'-deoxycytidine (5AZA-CdR), a potent inhibitor of DNA methylation, in combination with an inhibitor of histone deacetylase (HDAC). RESULTS:Here, we used a clonogenic assay to evaluate the in vitro antineoplastic activity of 5AZA-CdR in combination with different HDAC inhibitors on EWS cells. We observed that the HDAC inhibitors, MS-275, trichostatin-A, phenylbutyrate, LAQ824 and depsipeptide, enhanced the antineoplastic action of 5AZA-CdR on EWS cells. The combination of 5AZA-CdR and MS-275 showed marked synergy, and was correlated with significant reactivation of the expression of two TSGs, E-cadherin and tumor suppressor lung cancer-1 (TSLC1), in a EWS cell line. CONCLUSION:These results suggest the value of future clinical studies investigating the combination of 5AZA-CdR and MS-275 in patients with advanced EWS.
| S-EPMC2600626 | biostudies-literature
Project description:Photodynamic therapy (PDT) of tumours is based on administration of a photosensitiser followed by irradiation of the tumour with visible light leading to production of reactive oxygen species that cause direct tumour cell death and vascular damage. PDT also initiates acute local inflammation, which facilitates the development of adaptive antitumour immunity. It has recently been reported that PDT can induce strong antitumour immunity towards tumours cells expressing P1A, tumour-associated antigen. Using four different tumour models, we show that antitumour immune response can be further improved when PDT is combined with a clinically approved epigenetic agent that induces expression of a silenced P1A antigen. Induction of P1A with 5-aza-2'-deoxycytidine, a methyltransferase inhibitor, resulted in potentiated antitumour effects in mice with Lewis lung carcinoma and 4T1 mammary carcinoma when combined with PDT treatment. In CT26 colon carcinoma and EMT6 mammary carcinoma models the combination therapy resulted in complete responses and long-term survival. All long-term surviving mice were resistant to re-inoculation with the same tumour cells. Antitumour efficacy of the combination treatment was severely impaired by depletion of CD8(+) cytotoxic T cells, whereas adoptive transfer of CD8(+) T cells from long-term surviving mice allowed for significant tumour growth delay in tumour-bearing mice. Taken together, these findings show that PDT leads to strong specific antitumour immune responses, and that epigenetic modification of tumour antigens levels may be a novel approach to further enhance the effectiveness of PDT. The present results provide a strong rationale for clinical development of this therapeutic approach.
| S-EPMC4136636 | biostudies-literature
Project description:Melanoma progression model
| S-ECPF-GEOD-1792 | biostudies-other
Project description:5 melanoma cell lines: MelJUSO, A375, 607B, 518A2, Skmel 28
| S-ECPF-GEOD-1845 | biostudies-other
Project description:Background: UV exposure-induced oxidative stress is implicated as the driving mechanism for melanoma. Increased oxidative stress results in DNA damage and epigenetic modifications. We wondered whether a low dose of antioxidant could attenuate the oxidative stress of and help cells respond to epigenetic modification treatment at a lower dose. Sulforaphane (SFN) is a natural bioactivated product of the cruciferous family and is known as an antioxidant. We investigated the combinational effect of SFN and epigenetic modification drug, 5-aza-2'-deoxycytidine (DAC), on metastatic melanoma growth. Methods: Cell growth characteristics, RNA-seq and histone post-translational modification markers (PTMs) were compared in single and combination treatments. Results: We found increased cell growth inhibition and changes in gene expression profiles which includes a key immuno-regulator cytokine, C-C motif ligand 5 (CCL-5) gene expression upon combinational treatments. There was no significant difference in detectable histone PTMs between treatments. Conclusions: These results indicate a potential combinational effect of a dietary antioxidant and an FDA-approved epigenetic drug in controlling melanoma growth. The long-term goal of the current study is to find the therapeutic role of the dietary antioxidant SFN as a supporting drug for targeted epigenetic treatment with DAC in controlling melanoma growth.
2019-02-28 | GSE127252 | GEO
Project description:63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. The aim of this study was to identify potential downstream targets of key oncogenes and TSGs in melanoma (including p14ARF, p16INK4A, BRAF etc). Publications relevant to this series include:; Johansson et al. Pigment Cell Res 2007. Experiment Overall Design: 63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. These cell lines were sequenced for key tumour suppressor genes (TSGs) and oncogenes known to be involved in melanoma development. The microarray data was then analysed together with a particular genotype status (see relevant publications) to identify genes that potentially act downstream of these oncogenes and TSGs to contribute to melanoma development. See publications for analysis methods.
| S-ECPF-GEOD-7127 | biostudies-other
Project description:T1 and G1 are the two melanoma cell lines, established from primary tumor (T1) and lymph node metastases (G1) of a 77 years old male patient. While G1 cells were resistant to TRAIL (TNF-related apoptosis-inducing ligand) mediated cell death, T1 cells exhibited a high dose- and time-dependent sensitivity to TRAIL. Cells were treated with or without of two doses (0.2 and 1ug/ml) of TRAIL for 24 h. Gene expression of each sample vs pool was measured. TRAIL-resistant metastatic G1 vs primary TRAIL-sensitive T1 was compared.
| S-ECPF-MEXP-247 | biostudies-other