Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136237 | ENA |
REPOSITORIES: ENA
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Project description:Melanoma growth is driven by malignant melanoma initiating cells (MMIC) identified by expression of the ATP-binding cassette (ABC) member, ABCB5. ABCB5+ melanoma subpopulations have been shown to overexpress the vasculogenic differentiation markers CD144 (VE-cadherin) and TIE-1 and are associated with CD31-negative vasculogenic mimicry (VM), an established biomarker associated with increased patient mortality. Here we identify a critical role for VEGFR-1 signaling in ABCB5+ MMIC-dependent VM and tumor growth. Global gene expression analyses, validated by mRNA and protein determinations, revealed preferential expression of VEGFR-1 on ABCB5+ tumor cells purified from clinical melanomas and established melanoma lines. In vitro, VEGF induced in a VEGFR-1-dependent manner expression of CD144 in ABCB5+ subpopulations that constitutively expressed VEGFR-1, but not in ABCB5- bulk populations that were predominantly VEGFR-1-negative. In vivo, melanomaspecific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5+ VM morphology and inhibited ABCB5+ VM-associated production of the secreted melanoma mitogen, laminin. Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >90%). Our results demonstrate that VEGFR-1 function in MMIC regulates VM and associated laminin production, and show that this function represents one mechanism through which MMIC promote tumor growth.
2011-01-13 | GSE26569 | GEO
Project description:Melanoma growth is driven by malignant melanoma initiating cells (MMIC) identified by expression of the ATP-binding cassette (ABC) member, ABCB5. ABCB5+ melanoma subpopulations have been shown to overexpress the vasculogenic differentiation markers CD144 (VE-cadherin) and TIE-1 and are associated with CD31-negative vasculogenic mimicry (VM), an established biomarker associated with increased patient mortality. Here we identify a critical role for VEGFR-1 signaling in ABCB5+ MMIC-dependent VM and tumor growth. Global gene expression analyses, validated by mRNA and protein determinations, revealed preferential expression of VEGFR-1 on ABCB5+ tumor cells purified from clinical melanomas and established melanoma lines. In vitro, VEGF induced in a VEGFR-1-dependent manner expression of CD144 in ABCB5+ subpopulations that constitutively expressed VEGFR-1, but not in ABCB5- bulk populations that were predominantly VEGFR-1-negative. In vivo, melanomaspecific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5+ VM morphology and inhibited ABCB5+ VM-associated production of the secreted melanoma mitogen, laminin. Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >90%). Our results demonstrate that VEGFR-1 function in MMIC regulates VM and associated laminin production, and show that this function represents one mechanism through which MMIC promote tumor growth. Microarray analyses were performed on purified ABCB5+ (n=5) and ABCB5- (n=5) cell subsets derived from the established human melanoma cell lines G3361 and A375 and from three distinct clinical melanoma specimen. Total RNA was extracted, processed and hybridized onto Affymetrix human HG-U133Plus2 GeneChip microarrays (Affymetrix, Santa Clara, CA).
2011-01-13 | E-GEOD-26569 | biostudies-arrayexpress
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Project description:Melanoma is a malignant tumor with a terrible prognosis. In this study, we showed regorafenib has the ability to limit the growth, invasion and metastasis of melanoma cells but to upregulate apoptosis-prompting markers (cleaved-PARP and Bax). Moreover, ERK/E2F3 signaling influences regorafenib's ability to suppress melanoma cell growth. Ultimately, regorafenib significantly inhibits tumor growth in a dose-dependent manner in vivo.
2024-09-06 | GSE273844 | GEO
Project description:Voluntary exercise reduces the risk of cancer and lowers the risk of disease recurrence. Yet the mechanisms for this protection remain to be elucidated. Here we demonstrate that exercise halves tumor growth through an exercise-dependent mobilization and intratumoral infiltration of NK cells in malignant melanoma. Using voluntary wheel running, we show that exercise prior to and during B16 tumor challenge reduced tumor growth by 67%, and this reduction was associated with increased inflammation and immune cell infiltrates, especially NK cells, in the tumors from exercising mice. Depletion of NK cells blunted the exercise-dependent reduction in tumor growth. Moreover, during exercise, NK cells were engaged through an epinephrine-dependent mobilization to the circulation and redistributed to peripheral tissues through an IL-6 dependent mechanism. This study highlights the importance of exercise-dependent immune regulation in the control of malignant melanoma Gene expression profile of melanoma tumor tissue from two groups of exercise and non-exercise mice
2016-07-21 | E-GEOD-62628 | biostudies-arrayexpress
Project description:Transcription profiling by array of human malignant peripheral nerve sheath tumor cells after infection with herpes simplex virus G207
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Project description:Over the last decades, exosomes have received increasing attention due to their involvement in numerous pathologies including cancer. Tumor-derived exosomes and exosomes derived from the tumor microenvironment are implicated in multiple mechanisms that support disease progression such as the escape of malignant cells from immunosurveillance, tumor cell growth, tumor angiogenesis, preparation of a pre-metastatic niche and remodeling of the extracellular matrix, thereby promoting dissemination and metastasis. Here, we performed protein expression phenotyping of exosomes derived from different invasive and proliferative melanoma cell lines (n=8) to provide a solid framework of gene expression programs, which - in a clinical setting - would be useful for prognosis and may also predict treatment response. Cell line characteristics have been published previously (Wenzina et al.,2020). Having identified a set of differentially expressed proteins in proliferative and invasive melanoma cell lines, we correlated them to the protein composition of plasma exosomes from melanoma patients pre and post immunotherapy treatment (n=7) as well as healthy controls (n=5).
2022-07-14 | PXD025475 | Pride
Project description:The acquisition of cell invasiveness is the key transition from benign melanocyte hyperplasia to aggressive melanoma. Recent work using non-melanoma cancer cells has provided an intriguing new link between the presence of supernumerary centrosomes and increased cell invasion. Moreover, supernumerary centrosomes were shown to drive non-cell-autonomous invasion of cancer cells. Although centrosomes are the principle microtubule organizing centers the role of dynamic microtubules for non-cell-autonomous invasion remains unexplored, in particular in melanoma. We investigated the role of supernumerary centrosomes and dynamic microtubules in melanoma cell invasion and found that highly invasive melanoma cells are characterized by the presence of supernumerary centrosomes and by increased microtubule growth rates, both of which are functionally interlinked. We demonstrate that enhanced microtubule growth is required for increased 3D melanoma cell invasion. Moreover, we show that the activity to enhance microtubule growth can be transferred to adjacent non-invasive cells through extracellular vesicles harboring HER2 that are required for increased cell invasion of melanoma cells into 3D matrices. Hence, our study suggests that suppressing microtubule growth, either directly using anti-microtubule drugs or through HER2 inhibitors might be therapeutically beneficial to inhibit cell invasiveness and thus, metastasis of malignant melanoma.
2022-04-27 | PXD032224 | Pride