2021
c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells
DÚCKA, Monika; Martina KUČERÍKOVÁ; Filip TRČKA; Jakub ČERVINKA; Elisabetta BIGLIERI et al.Základní údaje
Originální název
c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells
Autoři
DÚCKA, Monika; Martina KUČERÍKOVÁ; Filip TRČKA; Jakub ČERVINKA; Elisabetta BIGLIERI; Jan ŠMARDA; Lubor BORSIG; Petr BENEŠ a Lucia KNOPFOVÁ
Vydání
Neoplasia, New York, Elsevier Inc. 2021, 1476-5586
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
10603 Genetics and heredity
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 6.218
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/21:00118896
Organizační jednotka
Přírodovědecká fakulta
UT WoS
EID Scopus
Klíčová slova anglicky
Breast cancer; c-Myb; IL1alpha; NF-kappaB; Inflammation; Transactivation
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 28. 4. 2022 09:15, Mgr. Marie Novosadová Šípková, DiS.
Anotace
V originále
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.
Návaznosti
| GJ17-08985Y, projekt VaV |
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| NV18-07-00073, projekt VaV |
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