SEMA3E-PLXND1 induced transcriptional changes in B16 melanocytes
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ABSTRACT:
PROVIDER: PRJNA783012 | ENA |
REPOSITORIES: ENA
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Project description:Exposure to SEMA3E cause an immediate but transient collapse in F-actin of B16 melanocytes expressing the receptor PLXND1. Concomitant signal transduction by activated PLXND1 receptor mediated via its GTPase activating domain has a role in adapting the melanocytes to its micro-environment. To analyse these adaptive transcriptional responses B16 melanocytes were treated with SEMA3E for 2h to study early responses and for 8h to study prolonged responses. Cytochalasin D (8h) was used to distinguish the effects brough about by cytoskeletal collapse alone.
2024-07-01 | GSE189438 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE11580: Time course RA-treatment of B16 mouse melanoma cells GSE11584: Melan-a mouse melanocytes vs. B16 mouse melanoma cells Keywords: SuperSeries Refer to individual Series
2008-07-31 | E-GEOD-11588 | biostudies-arrayexpress
Project description:Gene expression profile of melan-a mouse melanocytes vs. B16 mouse melanoma cells. Keywords: Cell type comparison
2008-07-31 | GSE11584 | GEO
Project description:Gene expression profile of melan-a mouse melanocytes vs. B16 mouse melanoma cells. Experiment Overall Design: Balanced block design with dye swap. Six biological replicates, one replicate per array.
2008-10-21 | E-GEOD-11584 | biostudies-arrayexpress
Project description:Melanocytes within benign human nevi are the paradigm for tumor suppressive senescent cells in a pre-malignant neoplasm. These cells typically contain mutations in either the BRAF or N-RAS oncogene and express markers of senescence, including p16. However, a nevus can contain 10s to 100s of thousands of clonal melanocytes and approximately 20-30% of melanoma are thought to arise in association with a pre-existing nevus. Neither observation is indicative of fail-safe senescence-associated proliferation arrest and tumor suppression. We set out to better understand the status of nevus melanocytes. Proliferation-promoting Wnt target genes, such as cyclin D1 and c-myc, were repressed in oncogene-induced senescent melanocytes in vitro, and repression of Wnt signaling in these cells induced a senescent-like state. In contrast, cyclin D1 and c-myc were expressed in many melanocytes of human benign nevi. Specifically, activated Wnt signalling in nevi correlated inversely with nevus maturation, an established dermatopathological correlate of clinical benignancy. Single cell analyses of lone epidermal melanocytes and nevus melanocytes showed that expression of proliferation-promoting Wnt targets correlates with prior proliferative expansion of p16-expressing nevus melanocytes. In a mouse model, activation of Wnt signaling delayed, but did not bypass, senescence of oncogene-expressing melanocytes, leading to massive accumulation of proliferation-arrested, p16-positive non-malignant melanocytes. We conclude that clonal hyperproliferation of oncogene-expressing melanocytes to form a nevus is facilitated by transient delay of senescence due to activated Wnt signaling. The observation that activation of Wnt signaling correlates inversely with nevus maturation, an indicator of clinical benignancy, supports the notion that persistent destabilization of senescence by Wnt signaling contributes to the malignant potential of nevi. We used RNA-Seq to detail the global programme of gene expression in primary human melanocytes which were Uninfected and BRAF600V induced cells
2013-08-01 | E-GEOD-46805 | biostudies-arrayexpress
Project description:Aims: CCND1 amplification was an unfavorable prognostic factor for patients with melanoma. This study aimed to investigate the molecular changes in tumor of B16 with CCND1 overexpression. Methods: High-throughput sequencing was used to identify genes that were differentially expressed in tumor between B16 controls and B16 with CCND1 overexpression. Tumors of B16 Ctrl (n=3) and B16 with CCND1 overexpression (n=3) were enrolled in this study. Results: mRNA expression of genes associated with immunity, such as CD8, Gzm, B2m, and Tap1 were decreased in tumors with CCND1 overexpression. Conclusion: CCND1 overexpression is associated with an immunosuppressive microenvironment.
2022-07-20 | GSE180327 | GEO
Project description:Analysis of gene expression patterns in cancer improved the understanding the mechanisms underlying the process of metastatic progression. Recent studies have attributed an important role to B-1 cells, a subset of B lymphocytes, in melanoma progression. It was already demonstrated that in vitro interaction between B16 melanoma cells and B-1 lymphocytes induced increase in metastatic potential of B16 lineage. In this study we used a microarray approach to assess gene expression profile in B16 melanoma cells after contacting B-1 lymphocytes (B16B1).
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Project description:Aspergillus fumigatus-induced transcriptional changes on murine eosinophils
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Project description:We wanted to correlate the protein cargo of secreted exosomes with gene expression pattern in B16-F1 and B16-F1R2. For that purpose, we performed RNA sequencing analysis of B16-F1, B16-F1R2 and B16-F1R2L (Fig.1E). We identified >3000 genes significantly up-regulated and >1000 significantly down-regulated in B16-F1R2 model compared to B16-F1, using a false discovery rate (FDR) of 0.05.
2021-07-28 | GSE150221 | GEO
Project description:Melanocytes within benign human nevi are the paradigm for tumor suppressive senescent cells in a pre-malignant neoplasm. These cells typically contain mutations in either the BRAF or N-RAS oncogene and express markers of senescence, including p16. However, a nevus can contain 10s to 100s of thousands of clonal melanocytes and approximately 20-30% of melanoma are thought to arise in association with a pre-existing nevus. Neither observation is indicative of fail-safe senescence-associated proliferation arrest and tumor suppression. We set out to better understand the status of nevus melanocytes. Proliferation-promoting Wnt target genes, such as cyclin D1 and c-myc, were repressed in oncogene-induced senescent melanocytes in vitro, and repression of Wnt signaling in these cells induced a senescent-like state. In contrast, cyclin D1 and c-myc were expressed in many melanocytes of human benign nevi. Specifically, activated Wnt signalling in nevi correlated inversely with nevus maturation, an established dermatopathological correlate of clinical benignancy. Single cell analyses of lone epidermal melanocytes and nevus melanocytes showed that expression of proliferation-promoting Wnt targets correlates with prior proliferative expansion of p16-expressing nevus melanocytes. In a mouse model, activation of Wnt signaling delayed, but did not bypass, senescence of oncogene-expressing melanocytes, leading to massive accumulation of proliferation-arrested, p16-positive non-malignant melanocytes. We conclude that clonal hyperproliferation of oncogene-expressing melanocytes to form a nevus is facilitated by transient delay of senescence due to activated Wnt signaling. The observation that activation of Wnt signaling correlates inversely with nevus maturation, an indicator of clinical benignancy, supports the notion that persistent destabilization of senescence by Wnt signaling contributes to the malignant potential of nevi.
2013-08-01 | GSE46805 | GEO