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Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma

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Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma. / Oliveira-Ferrer, Leticia; Milde-Langosch, Karin; Eylmann, Kathrin; Rossberg, Maila; Müller, Volkmar; Schmalfeldt, Barbara; Witzel, Isabell; Wellbrock, Jasmin; Fiedler, Walter.

in: INT J MOL SCI, Jahrgang 21, Nr. 2, 17.01.2020.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Oliveira-Ferrer, L, Milde-Langosch, K, Eylmann, K, Rossberg, M, Müller, V, Schmalfeldt, B, Witzel, I, Wellbrock, J & Fiedler, W 2020, 'Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma', INT J MOL SCI, Jg. 21, Nr. 2. https://doi.org/10.3390/ijms21020602

APA

Oliveira-Ferrer, L., Milde-Langosch, K., Eylmann, K., Rossberg, M., Müller, V., Schmalfeldt, B., Witzel, I., Wellbrock, J., & Fiedler, W. (2020). Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma. INT J MOL SCI, 21(2). https://doi.org/10.3390/ijms21020602

Vancouver

Oliveira-Ferrer L, Milde-Langosch K, Eylmann K, Rossberg M, Müller V, Schmalfeldt B et al. Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma. INT J MOL SCI. 2020 Jan 17;21(2). https://doi.org/10.3390/ijms21020602

Bibtex

@article{e60799c6dc214c9eb1d3a0bc23db27f9,
title = "Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma",
abstract = "During the last few years, diverse studies have shown that tumors can actively interact with the lymphatic system and promote metastases development. In order to examine the molecular mechanisms involved in this interaction, we co-cultured tumor and lymphatic endothelial cells (LEC) and subsequently analyzed the molecular alterations of LECs. Therefore, LECs were co-cultivated with either a highly or weakly metastatic breast cancer cell line using contact (mixture) and non-contact (transwell) co-cultures. mRNA profiles from LECs were subsequently analyzed for genes specifically induced by highly metastatic tumor cells ({"}metastatic specific{"}). Among the up-regulated {"}metastatic specific{"} genes, we found candidates involved in cell cycle, cell adhesion and motility (BST2, E-selectin, and HMMR), cytokines (CCL7, CXCL6, CXCL1, and CSF2) and factors of the complement system (C1R, C3, and CFB). Among the down-regulated genes, we detected the hyaluronan receptor STAB2, angiogenic factor apelin receptor (APLNR), and the glycosylation enzyme MAN1A1. In an additional prostate cancer co-culture model, we could confirm a {"}metastatic specific{"} upregulation of E-selectin and CCL7 in LECs after interaction with the prostate cancer cell lines LNCAP (highly metastatic) and DU145 (weakly metastatic). These data allowed us to identify a set of genes regulated in LECs during in vitro communication with cancer cells, which might subsequently facilitate lymphatic metastasis.",
author = "Leticia Oliveira-Ferrer and Karin Milde-Langosch and Kathrin Eylmann and Maila Rossberg and Volkmar M{\"u}ller and Barbara Schmalfeldt and Isabell Witzel and Jasmin Wellbrock and Walter Fiedler",
year = "2020",
month = jan,
day = "17",
doi = "10.3390/ijms21020602",
language = "English",
volume = "21",
journal = "INT J MOL SCI",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "2",

}

RIS

TY - JOUR

T1 - Mechanisms of Tumor-Lymphatic Interactions in Invasive Breast and Prostate Carcinoma

AU - Oliveira-Ferrer, Leticia

AU - Milde-Langosch, Karin

AU - Eylmann, Kathrin

AU - Rossberg, Maila

AU - Müller, Volkmar

AU - Schmalfeldt, Barbara

AU - Witzel, Isabell

AU - Wellbrock, Jasmin

AU - Fiedler, Walter

PY - 2020/1/17

Y1 - 2020/1/17

N2 - During the last few years, diverse studies have shown that tumors can actively interact with the lymphatic system and promote metastases development. In order to examine the molecular mechanisms involved in this interaction, we co-cultured tumor and lymphatic endothelial cells (LEC) and subsequently analyzed the molecular alterations of LECs. Therefore, LECs were co-cultivated with either a highly or weakly metastatic breast cancer cell line using contact (mixture) and non-contact (transwell) co-cultures. mRNA profiles from LECs were subsequently analyzed for genes specifically induced by highly metastatic tumor cells ("metastatic specific"). Among the up-regulated "metastatic specific" genes, we found candidates involved in cell cycle, cell adhesion and motility (BST2, E-selectin, and HMMR), cytokines (CCL7, CXCL6, CXCL1, and CSF2) and factors of the complement system (C1R, C3, and CFB). Among the down-regulated genes, we detected the hyaluronan receptor STAB2, angiogenic factor apelin receptor (APLNR), and the glycosylation enzyme MAN1A1. In an additional prostate cancer co-culture model, we could confirm a "metastatic specific" upregulation of E-selectin and CCL7 in LECs after interaction with the prostate cancer cell lines LNCAP (highly metastatic) and DU145 (weakly metastatic). These data allowed us to identify a set of genes regulated in LECs during in vitro communication with cancer cells, which might subsequently facilitate lymphatic metastasis.

AB - During the last few years, diverse studies have shown that tumors can actively interact with the lymphatic system and promote metastases development. In order to examine the molecular mechanisms involved in this interaction, we co-cultured tumor and lymphatic endothelial cells (LEC) and subsequently analyzed the molecular alterations of LECs. Therefore, LECs were co-cultivated with either a highly or weakly metastatic breast cancer cell line using contact (mixture) and non-contact (transwell) co-cultures. mRNA profiles from LECs were subsequently analyzed for genes specifically induced by highly metastatic tumor cells ("metastatic specific"). Among the up-regulated "metastatic specific" genes, we found candidates involved in cell cycle, cell adhesion and motility (BST2, E-selectin, and HMMR), cytokines (CCL7, CXCL6, CXCL1, and CSF2) and factors of the complement system (C1R, C3, and CFB). Among the down-regulated genes, we detected the hyaluronan receptor STAB2, angiogenic factor apelin receptor (APLNR), and the glycosylation enzyme MAN1A1. In an additional prostate cancer co-culture model, we could confirm a "metastatic specific" upregulation of E-selectin and CCL7 in LECs after interaction with the prostate cancer cell lines LNCAP (highly metastatic) and DU145 (weakly metastatic). These data allowed us to identify a set of genes regulated in LECs during in vitro communication with cancer cells, which might subsequently facilitate lymphatic metastasis.

U2 - 10.3390/ijms21020602

DO - 10.3390/ijms21020602

M3 - SCORING: Journal article

C2 - 31963450

VL - 21

JO - INT J MOL SCI

JF - INT J MOL SCI

SN - 1661-6596

IS - 2

ER -