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Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

ABSTRACT: Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

PROVIDER: PRJNA732077 | ENA |

REPOSITORIES: ENA

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Gene expression profiling following the overexpression or the knockdown of Ambra1 in A375 melanoma cell lines

Project description:Melanoma is the most deadly type of skin cancers and, there is a continuous need to develop early biomarkers as well as treatments to improve the survivability of patients. Ambra1 is an essential regulator in autophagy and it has been recently shown to have a role in cell proliferation. We used microarrays to analyse the transcriptomic changesi n A375 melanoma cell lines following Ambra1 differential expression

2021-05-23 | GSE175361 | GEO

Cytoglobin overexpression-dependent transcriptomic changes in A375 melanoma cells

Project description:Cytoglobin overexpression-dependent transcriptomic changes in A375 melanoma cells

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Analysis of gene expression profiles of human melanoma A375 cells with or without CD10 overexpression

Project description:Analysis of effect of CD10 in melanoma at gene expression level. The hypothesis tested in the present study was that CD10 promotes melanoma tumor progression. Results provide important information of the significant gene expression change between CD10-transfected and mock-transfected A375 cells, such as significantly increased genes included those related to anti-apoptosis, angiogenesis and cell proliferation. Total RNA obtained from CD10-transfected A375 melanoma cells was that from compared to mock-transfected A375 cells.

2014-10-18 | E-GEOD-62464 | biostudies-arrayexpress

Cytoglobin overexpression-dependent transcriptomic changes in A375 melanoma cells

Project description:Cytoglobin (CYGB) is a member of the oxygen-binding globin superfamily. In this study, we comprehensively explored the CYGB-dependent transcriptome in A375 melanoma cells overexpressing CYGB. Our findings reveal that CYGB overexpression positively enriches cancer-associated pathways, including the mTORC1 and AKT/mTOR signaling pathways, which are frequently overactivated in tumors. Moreover, several cancer-associated pathways, such as epithelial-mesenchymal transition (EMT) mediated by CSPG4, were downregulated upon CYGB overexpression. Intriguingly, our results indicate that CYGB overexpression leads to a reduction in the inflammatory state of melanoma cells. This anti-inflammatory potential is exemplified by the downregulation of key inflammasome-associated genes, including NLRP1, CASP1, and CD74, which play pivotal roles in cytokine regulation and inflammasome activation. Consistent with established globin functions, CYGB appears to play a crucial role in redox homeostasis. Furthermore, our study highlights CYGB's involvement in DNA repair mechanisms and its regulation of NOX4, reinforcing its versatility in safeguarding genomic integrity. Collectively, our data illuminate the diverse functions of CYGB in melanoma cells, pointing to its roles in cellular protection against oxidative stress, inflammation, and cancer-associated pathways. These findings pave the way for further research into the physiological role of CYGB and its potential as a therapeutic target in melanoma.

2024-08-21 | GSE241816 | GEO

Expression data from A375 melanoma parental and persister cells

Project description:Identify transcriptionnally and translationally regulated mRNA in melanoma parental and persister cells In this dataset, we include expression data of A375 melanoma drug-naïve parental cells and A375 melanoma persister cells that survived from BRAF and MEK inhibition. The expression data are studied in both total RNA and polysome-bounded RNA.

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A375 melanoma cells treated with leflunomide 25uM

Project description:Human A375 melanoma cells were treated with leflunomide 25uM for 3 days, then RNA harvested 6 arrays

2011-03-30 | E-GEOD-24526 | biostudies-arrayexpress

A375 melanoma cells treated with leflunomide 25uM

Project description:Human A375 melanoma cells were treated with leflunomide 25uM for 3 days, then RNA harvested

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NFATC2 knock-down on melanoma cell line A375

Project description:RNA-seq on NFATC2 knock-down (siRNA) on melanoma cell line A375

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Expression data from catalase stably transfected A375 human melanoma cells

Project description:Reactive oxygen species (ROS) are implicated in tumor transformation by modulating proteins involved in differentiation, proliferation and invasion. In order to identify genes that may support melanoma progression or regression after an antioxidant system (AOS) response, we developed and characterized a human melanoma cell model with different levels of ROS by stably overexpressing the antioxidant enzyme catalase in A375 amelanotic melanoma cells, and whole genome gene expression patterns were analyzed by microarrays. We used gene expression microarrays to study the AOS global response to catalase overexpression and to identify up-regulated and down-regulated genes during progression or regression of melanoma.

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Next generation sequencing of A375 melanoma cell line revealed a complex regulatory network when IGFBP5 overexpressed

Project description:IGFBP5, a critical regulators of insulin-like growth factors, has been reported to be involved in many kinds of carcinogenesis and cancer metastases. The role of IGFBP5 in human malignant melanoma (MM), however, remains largely unknown. In this study, we demonstrated that IGFBP5 was aberrantly expressed in human melanoma cells and cancer tissues. Overexpression of IGFBP5 dramatically inhibited the proliferation, migration and invasion of human melanoma cells, whereas knockdown of IGFBP5 by shRNA resulted in the opposite effects, enhanced the cell proliferation, migration and metastasis. In addition, IGFBP5 overexpression suppressed the growth and metastasis of melanoma xenograft tumor in vivo and IGFBP5 overexpression inhibited epithelialâmesenchymal transition (EMT) phenotype and stem cell property of tumor cell, with decreased expression of HIF1Î±, E-cadherin and stem cell markers NANOG, SOX2, OCT4, KLF4 and CD133. Moreover, IGFBP5 exhibited its growth inhibitory activity through inhibition of extracellular signal-regulated Kinase (ERK) and P38-MAPK signaling pathway. Taken together, our findings indicate that IGFBP5 acts as tumor suppressor roles in MM through the modulation of ERK1/2 and P38-MAPK signaling pathway as well as EMT procession and cell stemness, suggesting IGFBP5 as a novel target for human melanoma diagnosis and therapy. mRNA profiles of IGFBP5 over expression (OE) in A375 and A375 cell line were generated using Ion torrent

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