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@article{1753458,
author = {Dúcka, Monika and Kučeríková, Martina and Trčka, Filip and Červinka, Jakub and Biglieri, Elisabetta and Šmarda, Jan and Borsig, Lubor and Beneš, Petr and Knopfová, Lucia},
article_location = {New York},
article_number = {3},
doi = {http://dx.doi.org/10.1016/j.neo.2021.01.002},
keywords = {Breast cancer; c-Myb; IL1alpha; NF-kappaB; Inflammation; Transactivation},
language = {eng},
issn = {1476-5586},
journal = {Neoplasia},
title = {c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells},
url = {https://doi.org/10.1016/j.neo.2021.01.002},
volume = {23},
year = {2021}
}
TY - JOUR
ID - 1753458
AU - Dúcka, Monika - Kučeríková, Martina - Trčka, Filip - Červinka, Jakub - Biglieri, Elisabetta - Šmarda, Jan - Borsig, Lubor - Beneš, Petr - Knopfová, Lucia
PY - 2021
TI - c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells
JF - Neoplasia
VL - 23
IS - 3
SP - 326-336
EP - 326-336
PB - Elsevier Inc.
SN - 14765586
KW - Breast cancer
KW - c-Myb
KW - IL1alpha
KW - NF-kappaB
KW - Inflammation
KW - Transactivation
UR - https://doi.org/10.1016/j.neo.2021.01.002
N2 - The transcription factor c-Myb can be involved in the activation of many genes with protumorigenic function; however, its role in breast cancer (BC) development is still under discussion. c-Myb is considered as a tumor-promoting factor in the early phases of BC, on the other hand, its expression in BC patients relates to a good prognosis. Previously, we have shown that c-Myb controls the capacity of BC cells to form spontaneous lung metastasis. Reduced seeding of BC cells to the lungs is linked to high expression of c-Myb and a decline in expression of a specific set of inflammatory genes. Here, we unraveled a c-Myb-IL1alpha-NF-kappaB signaling axis that takes place in tumor cells. We report that an overexpression of c-Myb interfered with the activity of NF-kappaB in several BC cell lines. We identified IL1alpha to be essential for this interference since it was abrogated in the IL1alpha-deficient cells. Overexpression of IL1alpha, as well as addition of recombinant IL1alpha protein, activated NF-kappaB signaling and restored expression of the inflammatory signature genes suppressed by c-Myb. The endogenous levels of c-Myb negatively correlated with IL1alpha on both transcriptional and protein levels across BC cell lines. We concluded that inhibition of IL1alpha expression by c-Myb reduces NF-kappaB activity and disconnects the inflammatory circuit, a potentially targetable mechanism to mimic the antimetastatic effect of c-Myb with therapeutic perspective.
ER -
DÚCKA, Monika, Martina KUČERÍKOVÁ, Filip TRČKA, Jakub ČERVINKA, Elisabetta BIGLIERI, Jan ŠMARDA, Lubor BORSIG, Petr BENEŠ a Lucia KNOPFOVÁ. c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells. \textit{Neoplasia}. New York: Elsevier Inc., 2021, roč.~23, č.~3, s.~326-336. ISSN~1476-5586. Dostupné z: https://dx.doi.org/10.1016/j.neo.2021.01.002.
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