c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F21%3A00118896" target="_blank" >RIV/00216224:14310/21:00118896 - isvavai.cz</a>

Alternative codes found

RIV/00159816:_____/21:00075098

Result on the web

<a href="https://doi.org/10.1016/j.neo.2021.01.002" target="_blank" >https://doi.org/10.1016/j.neo.2021.01.002</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.neo.2021.01.002" target="_blank" >10.1016/j.neo.2021.01.002</a>

Result language

angličtina

Original language name

c-Myb interferes with inflammatory IL1alpha-NF-kappaB pathway in breast cancer cells

Original language description

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.

Czech name

—

Czech description

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Type

J_SC - Article in a specialist periodical, which is included in the SCOPUS database

CEP classification

—

OECD FORD branch

10603 - Genetics and heredity (medical genetics to be 3)

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2021

Confidentiality

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

Name of the periodical

Neoplasia

ISSN

1476-5586

e-ISSN

1476-5586

Volume of the periodical

23

Issue of the periodical within the volume

3

Country of publishing house

US - UNITED STATES

Number of pages

11

Pages from-to

326-336

UT code for WoS article

000623868500004

EID of the result in the Scopus database

2-s2.0-85101178278