Atlas of lymphangiogenesis
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ABSTRACT:
PROVIDER: PRJNA778399 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Atlas of lymphangiogenesis [scRNA-Seq]
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Project description:Atlas of lymphangiogenesis [scATAC-Seq]
| PRJNA778402 | ENA
Project description:During development, lymphatic vasculature forms as a second and distinct network that derives from embryonic blood vessels. Transdifferentiation of venous endothelial cells into specified lymphatic endothelial cells (LECs) is the first step in this process. Transdifferentiation and specification of LEC fate requires Prox1, but how Prox1 regulates transdifferentiation and differentiation is not fully understood. We present a single cell transcriptomic atlas of lymphangiogenesis spanning four key developmental stages that reveals new markers and functional regulators of lymphatic development. We extend this to comprehensively profile single cell transcriptomic and chromatin changes controlled by Prox1 using zygotic prox1a mutants, which form lymphatics that then dedifferentiate. Combining this with single cell analysis of Prox1-null, double prox1a/prox1b maternal zygotic mutants, we reveal in depth the role of Prox1 in control of LEC fate specification and differentiation. This resource reveals dual and progressive functions for Prox1, blocking blood vascular and hematopoietic fate while simultaneously up-regulating a small number of early acting genes that include tspan18a/b and lgals3a/b which are essential for lymphangiogenesis. This embryonic developmental resource will serve as a baseline to better understand both developmental and pathological lymphangiogenesis in the future. [Citations in sample metadata correspond to reference numbers in the associated publication.]
2023-04-27 | GSE188340 | GEO
Project description:During development, lymphatic vasculature forms as a second and distinct network that derives from embryonic blood vessels. Transdifferentiation of venous endothelial cells into specified lymphatic endothelial cells (LECs) is the first step in this process. Transdifferentiation and specification of LEC fate requires Prox1, but how Prox1 regulates transdifferentiation and differentiation is not fully understood. We present a single cell transcriptomic atlas of lymphangiogenesis spanning four key developmental stages that reveals new markers and functional regulators of lymphatic development. We extend this to comprehensively profile single cell transcriptomic and chromatin changes controlled by Prox1 using zygotic prox1a mutants, which form lymphatics that then dedifferentiate. Combining this with single cell analysis of Prox1-null, double prox1a/prox1b maternal zygotic mutants, we reveal in depth the role of Prox1 in control of LEC fate specification and differentiation. This resource reveals dual and progressive functions for Prox1, blocking blood vascular and hematopoietic fate while simultaneously up-regulating a small number of early acting genes that include tspan18a/b and lgals3a/b which are essential for lymphangiogenesis. This embryonic developmental resource will serve as a baseline to better understand both developmental and pathological lymphangiogenesis in the future. [Citations in sample metadata correspond to reference numbers in the associated publication.]
2023-04-27 | GSE188341 | GEO
Project description:1. To determine the association between LVD and clinico-pathologic variables in archived colorectal cancer and Nasopharyngeal carcinoma specimens
2. To determine the association between VEGF-C,-D expression with COX-2 expression and clinico-pathologic variables in colorectal cancer and Nasopharyngeal carcinoma
3. To determine the effect of celecoxib on lymphangiogenesis in Nasopharyngeal carcinoma Lymphangiogenesis and factors modulating lymphangiogenesis are associated with clinico-pathological outcome in Nasopharyngeal carcinoma and colorectal cancer. Celecoxib down-regulates lymphangiogenesis Archival colorectal cancer and Nasopharyngeal carcinoma tumor specimens will be obtained from the Department of Pathology. To determine the effect of celecoxib on lymphangiogenesis in Nasopharyngeal carcinoma, the investigators intend to analyze archived specimens collected in a previously conducted study. Colorectal tumor and nodal specimens and Nasopharyngeal carcinoma primary will be examined for MVD, LVD and growth factor expression using established haematoxylin and eosin and immunohistochemical techniques. Quantification of LVD and MVD shall be performed by two pathologists blinded to clinico-pathological variables using standardised methods.
| 2075499 | ecrin-mdr-crc
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-04-27 | GSE188342 | GEO
Project description:Prostate cancer is the most common cancer in men and is often associated with distant metastasis in its later stages. Lymphangiogenesis has been identified as a critical factor in cancer metastasis, and the adipokine apelin has been implicated in cancer progression and metastasis. However, researchers have yet to elucidate the mechanisms by which apelin regulates the key lymphangiogenic factor, Vascular Endothelial Growth Factor-C (VEGF-C), to promote distant metastasis in prostate cancer. This study identified a strong positive correlation between apelin levels and prostate cancer metastasis. Apelin stimulation was shown to upregulate VEGF-C expression, promoting the formation of new lymphatic vessels. Apelin treatment was also shown to downregulate miR-196a-5p expression via the proto-oncogene tyrosine kinase c-Src (c-Src) and Signal transducer and activator of transcription 3 (STAT3) signaling pathways, which regulates VEGF-C expression and lymphangiogenesis in prostate cancer cell lines. In an orthotopic mouse model, apelin inhibition prevented lymphangiogenesis and distant metastasis. These findings suggest that targeting apelin could be a promising therapeutic approach to preventing prostate cancer metastasis and lymphangiogenesis
2024-11-09 | GSE281393 | GEO
Project description:Unique functions for Notch4 in murine embryonic lymphangiogenesis
| PRJNA761427 | ENA
Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in the establishment of lymph node pre-metastatic niches by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and were taken up by lymphatic endothelial cells, reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. We found that neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells, inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended the survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support the idea that NGFR secreted in sEVs favors lymph node pre-metastatic niche formation and lymph node metastasis in melanoma
2021-08-05 | PXD024852 | Pride
Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in establishing the lymph node pre-metastatic niche by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and are taken up by lymphatic endothelial cells reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. Analysis of involved factors demonstrated that the neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended mice survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support that NGFR is secreted in sEVs favoring lymph node pre-metastatic niche formation and lymph node metastasis in melanoma.
2021-07-16 | PXD024108 | Pride