Effect of MDK expressing Melanoma cells conditioned media in Human LEC
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE94549 | GEO | 2017/06/27
SECONDARY ACCESSION(S): PRJNA371460
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression analysis in HLECs treated with gain of function of MDK in human Cervical Cancer cells(MS751) .
2024-04-16 | GSE263143 | GEO
Project description:Effect of MDK expressing Cervical Cancer cells(MS751) conditioned media in Human LEC
| PRJNA1095975 | ENA
Project description:RNA sequencing to analyze the gene expression changes in the WM852 and Bowes melanoma cells upon their co-culture with lymphatic endothelial cells (LECs). Platforms: NextSeq500 sequencer (Illumina) as quadruplicates
2018-05-01 | GSE100269 | GEO
Project description:Molecular function of BMPs in metastatic melanoma progression is undefined. The goal of this study is to identify BMP6-activated gene signaturs associated with metastatic progresses in human cutaneous melanoma. Transcriptome profiles (RNA-seq) of three melanoma cell lines (WM1341D, WM983B, and 1205Lu) stably expressing BMP6 and coressponding control cells were generated by deep sequencing using illumona HiSeq and mapped more than 30 million sequencing reads per sample to the human genome (build Hg19). Gene signatures down-regulated by BMP6 are mostly associated with extracellular matrix organization and growth factor binding, suggesting a metastasis-suppressive role of BMP6 in melanoma.
2021-01-10 | GSE164495 | GEO
Project description:We performed gain-of-function (GoF) and loss-of-function (LoF) analyses of Midkine in melanoma cells by RNA-seq.
2020-10-15 | GSE131203 | GEO
Project description:Malignant melanoma is a complex genetic disease and the most aggressive form of skin cancer. Melanoma progression and metastatic dissemination fundamentally relies on the process of angiogenesis. Melanomas produce an array of angiogenic modulators that mediate pathological angiogenesis. Such tumor-associated modulators arbitrate the enhanced proliferative, survival and migratory responses exhibited by endothelial cells, in the hypoxic tumor environment. The current study focuses on melanoma-induced survival of endothelial cells under hypoxic conditions. Melanoma conditioned media were capable of enabling prolonged endothelial cell survival under hypoxia, in contrast with the conditioned media derived from melanocytes, breast and pancreatic tumors. To identify the global changes in gene expression and further characterize the pro-survival pathway induced in endothelial cells, we performed microarray analysis on endothelial cells treated with melanoma conditioned medium under normoxic and hypoxic conditions. Huvec cells were grown in melanoma conditioned medium or DMEM 10% FCS for 12 h under hypoxic or normoxic conditions. In order to identify the transcripts modulated by melanoma CM, samples treated with MCM were compared to those grown in DMEM alone.
2013-09-30 | E-GEOD-33115 | biostudies-arrayexpress
Project description:Malignant melanoma is a complex genetic disease and the most aggressive form of skin cancer. Melanoma progression and metastatic dissemination fundamentally relies on the process of angiogenesis. Melanomas produce an array of angiogenic modulators that mediate pathological angiogenesis. Such tumor-associated modulators arbitrate the enhanced proliferative, survival and migratory responses exhibited by endothelial cells, in the hypoxic tumor environment. The current study focuses on melanoma-induced survival of endothelial cells under hypoxic conditions. Melanoma conditioned media were capable of enabling prolonged endothelial cell survival under hypoxia, in contrast with the conditioned media derived from melanocytes, breast and pancreatic tumors. To identify the global changes in gene expression and further characterize the pro-survival pathway induced in endothelial cells, we performed microarray analysis on endothelial cells treated with melanoma conditioned medium under normoxic and hypoxic conditions.
2013-09-30 | GSE33115 | GEO
Project description:Human melanoma MeWo cells and their respective LM2 metastatic derivatives, generated through in vivo selection, were transcriptomically profiled in the context of miR-199a and miR-1908 gain- and loss-of-function in order to identify putative target genes for these miRNAs, MeWo cells and their respective LM2 metastatic derivatives in the context of miR-199a and miR-1908 gain- and loss-of-function
2013-02-10 | E-GEOD-35668 | biostudies-arrayexpress
Project description:Epigenetic regulators have emerged as critical factors governing the biology of cancer. Here, in the context of melanoma, we show that RNF2 is prognostic, exhibiting progression-correlated expression in human melanocytic neoplasms. Through a series of gain of function and loss of function studies, we establish that RNF2 is oncogenic and pro-metastatic. Mechanistically, RNF2-mediated invasive behavior is dependent on its ability to mono-ubiquitinate H2AK119 at the promoter of LTBP2, resulting in silencing of this negative regulator of TGFβ signaling. In contrast, RNF2's oncogenic activity did not require its catalytic activity nor derives from its canonical gene repression function, rather RNF2 drives proliferation through direct transcriptional up-regulation of the cell cycle regulator CCND2. In summary, RNF2 regulates distinct biological processes in the genesis and progression of melanoma via distinct molecular mechanisms, underscoring the complex and multi-faceted actions of epigenetic regulators in cancer. RNF2 is overexpressed in immortalized human melanocytes HMEL-BRAFV600E to address impact of RNF2 overexpression in melanoma and identify RNF2 target genes. ChIP was performed to identify RNF2 binding sites using antibody against the V5 tag.
2016-07-03 | E-GEOD-51929 | biostudies-arrayexpress
Project description:Here, we investigated the effect of conditioned media (CM) obtained from cultured mouse DRG neurons on Tppp3+ cells, mainly on proliferation and differentiation potential. Peripheral afferent neurons terminate at the surfaces of tendons, yet their role after injury beyond nociceptive functions remain unclear. Using transgenic animal models, sensory neurons were found to sprout after Achilles tendon injury in domains of Nerve growth factor (NGF) expression. Conditional deletion of Ngf in either myeloid or mesenchymal cell types led to tendon repair defects – findings phenocopied by inactivation of TrkA (Tropomyosin receptor kinase A) using a knockin mouse model. A combination of spatial and single cell transcriptomics revealed dysregulated inflammatory and TGF signaling upon lack of neural input. Utilizing sural nerve transection in reporter animals, we identified that neural input is required for proper expansion of Tppp3+ tendon sheath progenitor cells (TSPCs) after injury, and in vitro approaches implicated TGF signaling activation in Tppp3+ TSPC neural response. Finally, in a translational approach, activation of TrkA+ sensory neurons using a partial agonist led to a significant increase in TGF signaling, TSPC expansion, and improved tendon repair. Collectively, these data implicate peripheral afferent neural networks in the coordinated acute tendon injury response, and identify candidate molecules to speed the reparative process.
2023-11-27 | GSE221035 | GEO