Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60461373%3A22310%2F24%3A43931115" target="_blank" >RIV/60461373:22310/24:43931115 - isvavai.cz</a>

Výsledek na webu

<a href="https://link.springer.com/content/pdf/10.1186/s12943-023-01922-8.pdf?utm_source=scopus&getft_integrator=scopus" target="_blank" >https://link.springer.com/content/pdf/10.1186/s12943-023-01922-8.pdf?utm_source=scopus&getft_integrator=scopus</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1186/s12943-023-01922-8" target="_blank" >10.1186/s12943-023-01922-8</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Popis výsledku v původním jazyce

In the early 1990&apos;s a group of unrelated genes were identified from the sites of recurring translocations in B-cell lymphomas. Despite sharing the nomenclature &apos;Bcl&apos;, and an association with blood-borne cancer, these genes have unrelated functions. Of these genes, BCL2 is best known as a key cancer target involved in the regulation of caspases and other cell viability mechanisms. BCL3 on the other hand was originally identified as a non-canonical regulator of NF-kB transcription factor pathways - a signaling mechanism associated with important cell outcomes including many of the hallmarks of cancer. Most of the early investigations into BCL3 function have since focused on its role in NF-kB mediated cell proliferation, inflammation/immunity and cancer. However, recent evidence is coming to light that this protein directly interacts with and modulates a number of other signaling pathways including DNA damage repair, WNT/beta-catenin, AKT, TGF beta/SMAD3 and STAT3 - all of which have key roles in cancer development, metastatic progression and treatment of solid tumours. Here we review the direct evidence demonstrating BCL3&apos;s central role in a transcriptional network of signaling pathways that modulate cancer biology and treatment response in a range of solid tumour types and propose common mechanisms of action of BCL3 which may be exploited in the future to target its oncogenic effects for patient benefit.

Název v anglickém jazyce

Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age

Popis výsledku anglicky

In the early 1990&apos;s a group of unrelated genes were identified from the sites of recurring translocations in B-cell lymphomas. Despite sharing the nomenclature &apos;Bcl&apos;, and an association with blood-borne cancer, these genes have unrelated functions. Of these genes, BCL2 is best known as a key cancer target involved in the regulation of caspases and other cell viability mechanisms. BCL3 on the other hand was originally identified as a non-canonical regulator of NF-kB transcription factor pathways - a signaling mechanism associated with important cell outcomes including many of the hallmarks of cancer. Most of the early investigations into BCL3 function have since focused on its role in NF-kB mediated cell proliferation, inflammation/immunity and cancer. However, recent evidence is coming to light that this protein directly interacts with and modulates a number of other signaling pathways including DNA damage repair, WNT/beta-catenin, AKT, TGF beta/SMAD3 and STAT3 - all of which have key roles in cancer development, metastatic progression and treatment of solid tumours. Here we review the direct evidence demonstrating BCL3&apos;s central role in a transcriptional network of signaling pathways that modulate cancer biology and treatment response in a range of solid tumour types and propose common mechanisms of action of BCL3 which may be exploited in the future to target its oncogenic effects for patient benefit.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30104 - Pharmacology and pharmacy

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2024

Kód důvěrnosti údajů

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

Název periodika

Molecular Cancer

ISSN

1476-4598

e-ISSN

1476-4598

Svazek periodika

2024

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

17

Strana od-do

—

Kód UT WoS článku

001138929200002

EID výsledku v databázi Scopus

2-s2.0-85181717712