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Project description:Mechanism of nonthermal plasma on melanoma cell growth suppression
| PRJNA986164 | ENA
Project description:To investigate the effect of UV on SOCE suppression in melanoma progression We performed gene expression analysis of cells exhibiting SOCE suppression and cells not exhibiting SOCE suppression compared to control
2022-06-17 | GSE205830 | GEO
Project description:Treatment of tumor progression and metastasis continues to be of major importance in the field of cancer. It is reported that cancer cells often show a pronounced sensitivity towards oxidative stress. Cold plasma offers the ability to deliver a delicate mix of reactive oxygen and nitrogen species directly into cells or tissues. Using a well-described argon plasma jet, we investigated the biological responses of plasma on tumor cell death, cell migration, and expression of adhesion-associated genes as well as cytoskeletal modifications. Using the human melanoma cancer cell line SK-Mel-147 we were able to show that plasma induced only little apoptosis but had profound effects on tumor cell motility. Plasma treatment of cells was associated with an inhibition of migration and disorganization of the actin cytoskeleton which were mediated through multiple signaling pathways, as transcriptome-wide gene analysis suggested. Specifically, changes in cell adhesion were regulated by differential expression of cell junction and cell-matrix proteins. These results provide evidence that plasma may be able to disturb the migration and adhesion in metastatic SK-Mel-147 cells. Microarrays were used to analyze and investigate the biological effects of cold plasma on human melanoma cell line SK-Mel-147. Using an argon plasma jet kinpen, regulated transcripts were analyzed and further described in Schmidt et al. (2015): M-bM-^@M-^\Human melanoma cell migration and adhesion is decreased by cold plasma treatmentM-bM-^@M-^]. A study using total RNA recovered from human SK-Mel-147, treated with cold plasma as well as H2O2-treated and untreated SK-Mel-147 controls.
2015-02-18 | E-GEOD-65972 | biostudies-arrayexpress
Project description:Treatment of tumor progression and metastasis continues to be of major importance in the field of cancer. It is reported that cancer cells often show a pronounced sensitivity towards oxidative stress. Cold plasma offers the ability to deliver a delicate mix of reactive oxygen and nitrogen species directly into cells or tissues. Using a well-described argon plasma jet, we investigated the biological responses of plasma on tumor cell death, cell migration, and expression of adhesion-associated genes as well as cytoskeletal modifications. Using the human melanoma cancer cell line SK-Mel-147 we were able to show that plasma induced only little apoptosis but had profound effects on tumor cell motility. Plasma treatment of cells was associated with an inhibition of migration and disorganization of the actin cytoskeleton which were mediated through multiple signaling pathways, as transcriptome-wide gene analysis suggested. Specifically, changes in cell adhesion were regulated by differential expression of cell junction and cell-matrix proteins. These results provide evidence that plasma may be able to disturb the migration and adhesion in metastatic SK-Mel-147 cells. Microarrays were used to analyze and investigate the biological effects of cold plasma on human melanoma cell line SK-Mel-147. Using an argon plasma jet kinpen, regulated transcripts were analyzed and further described in Schmidt et al. (2015): “Human melanoma cell migration and adhesion is decreased by cold plasma treatment”.
2015-02-18 | GSE65972 | GEO
Project description:The members of the eukaryotic chaperonin family are essential for cell survival. The dysregulation of chaperonin-containing TCP-1 subunit 3 (CCT3) is implicated in the development of several types of malignant tumors. However, its functional role in melanoma remains unknown. Herein, we elucidated the functional contribution of CCT3 to melanoma progression. The results indicated that CCT3 was frequently upregulated in melanoma tissues, and high level of CCT3 is correlated with clinical stage in melanoma patients. Knockdown of CCT3 in melanoma cells markedly inhibited cell proliferation and induced cell apoptosis in vitro and suppressed tumorigenesis in a mouse xenograft model. We also identified the cyclin-dependent kinase 1 (CDK1) as a downstream effector of CCT3 and further evaluation demonstrated that suppression of CCT3 attenuates cell proliferation via downregulating CDK1 expression and CCT3-mediated regulation of cell cycle signaling pathway in melanoma. Collectively, our results provide compelling evidence that CCT3 contributes to melanoma progression via CDK1 and is a potential therapeutic target for melanoma A-375 cells infected with NC lentivirus and CCT3 knockdown lentivirus were prepeared and cultured for RNA extraction and hybridization on Affymetrix microarrays.
2020-02-06 | GSE144788 | GEO
Project description:Suppression of Ca2+ Signaling Enhances Melanoma Progression
| PRJNA847914 | ENA
Project description:PGC1a is a transcriptional coactivator that regulates energy metabolism. PGC1a is highly expressed in a subset of melanoma tumors and cell lines. We generated gene-expression profile of control and PGC1alpha depleted A375P melanoma cells, a melanoma cell line that expresses very high levels of PGC1a to investigate the role of this gene in melanoma.
2013-02-25 | GSE36879 | GEO
Project description:Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma
| PRJNA604922 | ENA
Project description:Using a chromatin regulator-focused shRNA library, we found that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes resistance to BRAF and MEK inhibitors. To investigate how SOX10 loss leads to drug resistance, we performed transcriptome sequencing (RNAseq) of both parental A375 (Ctrl. PLKO) and A375-SOX10KD (shSOX10-1, shSOX10-2) cells. To ask directly whether SOX10 is involved indrug resistance in BRAF(V600E) melanoma patients, we isolated RNA from paired biopsies from melanoma patients (pre- and post- treatment) , that had gained BRAF or MEK inhibitor resistance . We performed RNAseq analysis to determine changes in transcriptome upon drug resistance. Investigate genes regulated by SOX10 and differntial gene expression between pre- and post-treatment biopsies. We use short hairpin RNA to suppression SOX10 in A375 cells and cells were harvested with trizol reagent for RNA isolation. For paired biopsies (patient samples) we collected the first biopsy before the initiation of treatment and the second biopsy after drug resistance developed. RNA was isolated from FFPE samples and subjected for RNA sequencing.
2014-01-04 | E-GEOD-50535 | biostudies-arrayexpress
Project description:We investigated the miRNAome in human melanocyte and melanoma cell lines using high-throughput RNA sequencing. We identified a group of dysregulated miRNAs by comparing the miRNA expression profiles among melanoma cell lines. Target genes of these miRNAs participate in functions associated with the cell cycle and apoptosis. Gene networks were built to investigate the interactions of genes during melanoma progression. We identified that the key genes that regulate melanoma cell proliferation were regulated by miRNAs. Our findings provide further knowledge regarding the mechanisms of melanoma development. miRNA profiles of melanocyte (HEMn-LP), low metastatic melanoma (A375) and high metastatic melanoma (A2058) cell line were generated using Illumina GA
2015-07-13 | E-GEOD-66823 | biostudies-arrayexpress