ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F25%3A00082387" target="_blank" >RIV/00159816:_____/25:00082387 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14110/25:00143288
Výsledek na webu
<a href="https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2025.1563969/full" target="_blank" >https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2025.1563969/full</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3389/fonc.2025.1563969" target="_blank" >10.3389/fonc.2025.1563969</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity
Popis výsledku v původním jazyce
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which epithelial-to-mesenchymal transition (EMT) plasticity is required for successful metastasis. ERK3 has been implicated in promoting breast cancer migration and invasion, but the mechanisms remain elusive. Here, we investigated ERK3 expression across patient-derived datasets and explored its role in promoting EMT plasticity using different 2D and 3D in vitro models to investigate cell-extracellular matrix adhesion, migration and invasion, anchorage-independent growth, extravasation and colonization. We have established an association between ERK3 overexpression and aggressive breast cancer phenotypes, higher tumour plasticity, as informed by its grade, and poor clinical outcomes. Based on the hypothesis that ERK3 contributes to TNBC progression by supporting a partial-EMT state, we showed that ERK3 contributes to different steps of the metastatic process, especially by enabling collective migration but also by modulating other functional aspects related to an active EMT program. In conclusion, our results demonstrate that ERK3 contributes to TNBC progression and potentially metastasis by promoting EMT plasticity and collective migration.
Název v anglickém jazyce
ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity
Popis výsledku anglicky
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, in which epithelial-to-mesenchymal transition (EMT) plasticity is required for successful metastasis. ERK3 has been implicated in promoting breast cancer migration and invasion, but the mechanisms remain elusive. Here, we investigated ERK3 expression across patient-derived datasets and explored its role in promoting EMT plasticity using different 2D and 3D in vitro models to investigate cell-extracellular matrix adhesion, migration and invasion, anchorage-independent growth, extravasation and colonization. We have established an association between ERK3 overexpression and aggressive breast cancer phenotypes, higher tumour plasticity, as informed by its grade, and poor clinical outcomes. Based on the hypothesis that ERK3 contributes to TNBC progression by supporting a partial-EMT state, we showed that ERK3 contributes to different steps of the metastatic process, especially by enabling collective migration but also by modulating other functional aspects related to an active EMT program. In conclusion, our results demonstrate that ERK3 contributes to TNBC progression and potentially metastasis by promoting EMT plasticity and collective migration.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30204 - Oncology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2025
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Frontiers in Oncology
ISSN
2234-943X
e-ISSN
—
Svazek periodika
15
Číslo periodika v rámci svazku
Aug 2025
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
22
Strana od-do
1563969
Kód UT WoS článku
001566876900001
EID výsledku v databázi Scopus
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