Transendothelial migration in breast cancer metastasis: when
does c-Myb step in?

a 2014

Transendothelial migration in breast cancer metastasis: when does c-Myb step in?

KNOPFOVÁ, Lucia, Petr BENEŠ, Michal MASAŘÍK, Pierre JURDIC, Jan ŠMARDA et. al.

Základní údaje

Originální název

Transendothelial migration in breast cancer metastasis: when does c-Myb step in?

Název česky

Transendoteliální migrace během metastázování prsních nádorů: kdy zasahuje protein c-Myb?

Autoři

KNOPFOVÁ, Lucia, Petr BENEŠ, Michal MASAŘÍK, Pierre JURDIC a Jan ŠMARDA

Vydání

ISREC2014 Metastatic colonization, Switzerland, 2014

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakt

Obor

Genetika a molekulární biologie

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Organizační jednotka

Přírodovědecká fakulta

Štítky

c-Myb, extravasation, metastasis, transendothelial migration

Změněno: 6. 1. 2015 13:57, Mgr. Lucia Knopfová, Ph.D.

Anotace

V originále

The process of metastasis requires multiple mutual interactions of tumor and stromal cells. Endothelial cells (ECs) encounter tumor cells in multiple steps of metastatic cascade: ECs are manipulated to form tumor vasculature, to provide permeable entry to secondary environment prior the arrival of metastatic cell, ECs participate in multiple tissue-specific adhesive interactions with tumor cells, and endothelium is eventually penetrated by tumor cells during intravasation/extravasation. Because of different structural features of blood vessels in different organs, the extravasation efficiency contributes to organ-specific pattern of metastatic spread. Our previous results show the organ-specific spread induced by the c-Myb transcription factor, the progenitor/stem cell regulator, in breast tumors. We described, that the Myb-overexpressing 4T1 mammary tumors in syngeneic BALB/c model rarely metastasized to lungs in contrast to control tumors, though the formation of the bone and liver metastases was not affected. We hypothesized that the selective disadvantage of these tumor cells in lung colonization might result from the deficiency in extravasation. We demonstrate here that capacity of transendothelial migration (TEM) of breast cancer cells in vitro is slightly reduced by overexpressed c-Myb. However, c-Myb does not affect the adhesion rate of breast carcinoma cells to EC monolayer. Analysis of publically available microarray data revealed that breast cancer cell lines capable of TEM (TEM+) express lower amounts of MYB mRNA than TEM- cell lines. We further investigated vascular permeability induced by soluble factors secreted from tumor cells by in vitro transwell assay, and visualized the events associated with cytoskeletal remodeling during TEM by fluorescence confocal microscopy. The altered tumor-EC interactions might participate in the c-Myb-induced site-selective spread of breast tumors.

Návaznosti

NT13441, projekt VaV

Název: Exprese proteinů rodiny Myb v adenokarcinomech tlustého střeva a vztah k jejich metastatickému potenciálu

Citovat

KNOPFOVÁ, Lucia, Petr BENEŠ, Michal MASAŘÍK, Pierre JURDIC a Jan ŠMARDA. Transendothelial migration in breast cancer metastasis: when does c-Myb step in? In ISREC2014 Metastatic colonization, Switzerland. 2014.

@proceedings{1161680,
   author = {Knopfová, Lucia and Beneš, Petr and Masařík, Michal and Jurdic, Pierre and Šmarda, Jan},
   booktitle = {ISREC2014 Metastatic colonization, Switzerland},
   language = {eng},
   title = {Transendothelial migration in breast cancer metastasis: when does c-Myb step in?},
   year = {2014}
}

TY  - CONF
ID  - 1161680
AU  - Knopfová, Lucia - Beneš, Petr - Masařík, Michal - Jurdic, Pierre - Šmarda, Jan
PY  - 2014
TI  - Transendothelial migration in breast cancer metastasis: when does c-Myb step in?
N2  - The process of metastasis requires multiple mutual interactions of tumor and stromal cells. Endothelial cells (ECs) encounter tumor cells in multiple steps of metastatic cascade: ECs are manipulated to form tumor vasculature, to provide permeable entry to secondary environment prior the arrival of metastatic cell, ECs participate in multiple tissue-specific adhesive interactions with tumor cells, and endothelium is eventually penetrated by tumor cells during intravasation/extravasation. Because of different structural features of blood vessels in different organs, the extravasation efficiency contributes to organ-specific pattern of metastatic spread. Our previous results show the organ-specific spread induced by the c-Myb transcription factor, the progenitor/stem cell regulator, in breast tumors. We described, that the Myb-overexpressing 4T1 mammary tumors in syngeneic BALB/c model rarely metastasized to lungs in contrast to control tumors, though the formation of the bone and liver metastases was not affected. We hypothesized that the selective disadvantage of these tumor cells in lung colonization might result from the deficiency in extravasation. We demonstrate here that capacity of transendothelial migration (TEM) of breast cancer cells in vitro is slightly reduced by overexpressed c-Myb. However, c-Myb does not affect the adhesion rate of breast carcinoma cells to EC monolayer. Analysis of publically available microarray data revealed that breast cancer cell lines capable of TEM (TEM+) express lower amounts of MYB mRNA than TEM- cell lines. We further investigated vascular permeability induced by soluble factors secreted from tumor cells by in vitro transwell assay, and visualized the events associated with cytoskeletal remodeling during TEM by fluorescence confocal microscopy. The altered tumor-EC interactions might participate in the c-Myb-induced site-selective spread of breast tumors.
ER  -

KNOPFOVÁ, Lucia, Petr BENEŠ, Michal MASAŘÍK, Pierre JURDIC a Jan ŠMARDA. Transendothelial migration in breast cancer metastasis: when does c-Myb step in? In \textit{ISREC2014 Metastatic colonization, Switzerland}. 2014.

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