ERK3/MAPK6 promotes triple-negative breast cancer progression
through collective migration and EMT plasticity

J 2025

ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity

MORAZZO, Sofia; Soraia FERNANDES; Marina FORTEA; Helena SKALOVA; Daniel PEREIRA DE SOUSA et al.

Základní údaje

Originální název

ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity

Autoři

Vydání

Frontiers in Oncology, LAUSANNE, FRONTIERS MEDIA SA, 2025, 2234-943X

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30204 Oncology

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 3.300 v roce 2024

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/25:00143305

Organizační jednotka

Lékařská fakulta

Klíčová slova anglicky

Triple-negative breast cancer (TNBC); Extracellular signal-regulated kinase 3 (ERK3); epithelial-to-mesenchymal transition (EMT); epithelial-mesenchymal plasticity (EMP); collective migration; mitogen-activated protein kinase 6 (MAPK6)

Štítky

14110132, 14110513, 14313050

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 14. 1. 2026 12:07, Mgr. Marie Novosadová Šípková, DiS.

Anotace

V originále

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.

Návaznosti

LM2018133, projekt VaV

Název: Český národní uzel Evropské infrastruktury pro translační medicínu (Akronym: EATRIS-ERIC-CZ)

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Involvement of Czech Translational Medicine Infrastructure to the European Advanced Translational Research Infrastructure in Medicine

Citovat

MORAZZO, Sofia; Soraia FERNANDES; Marina FORTEA; Helena SKALOVA; Daniel PEREIRA DE SOUSA; Marco CASSANI; Kamila VRZALOVÁ; Filip KAFKA; Jan VRBSKY; Mathilde SOULEZ; Sylvain MELOCHE; Ole MORTEN-SETERNES; Veronika BOSÁKOVÁ; Jaeyoung SHIN; Jan FRIČ; Kristina HAASE a Giancarlo FORTE. ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity. Frontiers in Oncology. LAUSANNE: FRONTIERS MEDIA SA, 2025, roč. 15, August, s. 1-22. ISSN 2234-943X. Dostupné z: https://doi.org/10.3389/fonc.2025.1563969.

@article{2547019,
   author = {Morazzo, Sofia and Fernandes, Soraia and Fortea, Marina and Skalova, Helena and Pereira de Sousa, Daniel and Cassani, Marco and Vrzalová, Kamila and Kafka, Filip and Vrbsky, Jan and Soulez, Mathilde and Meloche, Sylvain and MortenandSeternes, Ole and Bosáková, Veronika and Shin, Jaeyoung and Frič, Jan and Haase, Kristina and Forte, Giancarlo},
   article_location = {LAUSANNE},
   article_number = {August},
   doi = {https://doi.org/10.3389/fonc.2025.1563969},
   keywords = {Triple-negative breast cancer (TNBC); Extracellular signal-regulated kinase 3 (ERK3); epithelial-to-mesenchymal transition (EMT); epithelial-mesenchymal plasticity (EMP); collective migration; mitogen-activated protein kinase 6 (MAPK6)},
   language = {eng},
   issn = {2234-943X},
   journal = {Frontiers in Oncology},
   title = {ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity},
   url = {https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2025.1563969/full},
   volume = {15},
   year = {2025}
}

TY  - JOUR
ID  - 2547019
AU  - Morazzo, Sofia - Fernandes, Soraia - Fortea, Marina - Skalova, Helena - Pereira de Sousa, Daniel - Cassani, Marco - Vrzalová, Kamila - Kafka, Filip - Vrbsky, Jan - Soulez, Mathilde - Meloche, Sylvain - Morten-Seternes, Ole - Bosáková, Veronika - Shin, Jaeyoung - Frič, Jan - Haase, Kristina - Forte, Giancarlo
PY  - 2025
TI  - ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity
JF  - Frontiers in Oncology
VL  - 15
IS  - August
SP  - 1-22
EP  - 1-22
PB  - FRONTIERS MEDIA SA
SN  - 2234943X
KW  - Triple-negative breast cancer (TNBC)
KW  - Extracellular signal-regulated kinase 3 (ERK3)
KW  - epithelial-to-mesenchymal transition (EMT)
KW  - epithelial-mesenchymal plasticity (EMP)
KW  - collective migration
KW  - mitogen-activated protein kinase 6 (MAPK6)
UR  - https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2025.1563969/full
N2  - 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.
ER  -

MORAZZO, Sofia; Soraia FERNANDES; Marina FORTEA; Helena SKALOVA; Daniel PEREIRA DE SOUSA; Marco CASSANI; Kamila VRZALOVÁ; Filip KAFKA; Jan VRBSKY; Mathilde SOULEZ; Sylvain MELOCHE; Ole MORTEN-SETERNES; Veronika BOSÁKOVÁ; Jaeyoung SHIN; Jan FRIČ; Kristina HAASE a Giancarlo FORTE. ERK3/MAPK6 promotes triple-negative breast cancer progression through collective migration and EMT plasticity. \textit{Frontiers in Oncology}. LAUSANNE: FRONTIERS MEDIA SA, 2025, roč.~15, August, s.~1-22. ISSN~2234-943X. Dostupné z: https://doi.org/10.3389/fonc.2025.1563969.

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