Procathepsin D mitogenic effect on breast cancer cells is mediated by the NFkB activation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F09%3A00028841" target="_blank" >RIV/00216224:14310/09:00028841 - isvavai.cz</a>

Výsledek na webu

—

DOI - Digital Object Identifier

—

Jazyk výsledku

angličtina

Název v původním jazyce

Procathepsin D mitogenic effect on breast cancer cells is mediated by the NFkB activation

Popis výsledku v původním jazyce

Procathepsin D (pCD) is overexpressed and secreted by several types of tumors including breast cancer. pCD affects multiple stages of tumor progression including proliferation, angiogenesis and apoptosis. We have previously shown that mitogenic effect ofpCD on cancer cells is mediated via its propeptide part (AP). However, the mechanism of pCD action on breast cancer cells is not known. In this study we demostrated an increased expression of NFkB luciferase reporter gene, translocation of p65 into cellnucleus, and phosphorylation of IkB in AP-treated MCF-7 breast cancer cells. Moreover, we confirmed that NFkB activity is essential for pro-mitogenic effect of pCD on MCF-7 cells using dominant negative IkB stable transfectants and pharmacological NFkBinhibitors. These results suggest that pharmacological inhibitors of NFkB may be useful for treatment of pCD-secreting tumors.

Název v anglickém jazyce

Procathepsin D mitogenic effect on breast cancer cells is mediated by the NFkB activation

Popis výsledku anglicky

Procathepsin D (pCD) is overexpressed and secreted by several types of tumors including breast cancer. pCD affects multiple stages of tumor progression including proliferation, angiogenesis and apoptosis. We have previously shown that mitogenic effect ofpCD on cancer cells is mediated via its propeptide part (AP). However, the mechanism of pCD action on breast cancer cells is not known. In this study we demostrated an increased expression of NFkB luciferase reporter gene, translocation of p65 into cellnucleus, and phosphorylation of IkB in AP-treated MCF-7 breast cancer cells. Moreover, we confirmed that NFkB activity is essential for pro-mitogenic effect of pCD on MCF-7 cells using dominant negative IkB stable transfectants and pharmacological NFkBinhibitors. These results suggest that pharmacological inhibitors of NFkB may be useful for treatment of pCD-secreting tumors.

Druh

O - Ostatní výsledky

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2009

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů