GRB2 promotes brain metastasis in HER2-positive breast cancer by regulating the Ras/MAPK pathway

Brain metastasis is emerging as the most serious concern for breast cancer patients. HER2-positive breast cancer is more prone to undergo brain metastasis than other subtypes; notably, there has been little improvement in the treatment of brain metastasis .Our study confirmed the relevance of HER2 status to brain metastasis risk via clinical data analysis and revealed that exerts GRB2 tumorigenic effects by regulating the Ras/MAPK pathway in vivo and in vitro. Both an in situ injection model and a direct cerebral injection model were used to explore the ability of GRB2 to promote the brain metastasis. Results indicated that HER2- positive is a risk factor for brain metastasis according to clinical data. GRB2 enhances proliferation, migration, and invasion while suppressing apoptosis in HER2-positive breast cancer cells in vitro, primarily by regulating phosphorylation and alternative splicing of key proteins within the Ras/MAPK pathway. Notably, tumor cells were able to cross the blood‒brain barrier in both models assessed in this study. Thus, GRB2 is an oncogenic factor that contributes to the malignancy of HER2-positive breast cancer, GRB2 and HER2 can synergistically promote tumor cell penetration of the blood‒brain barrier and induce metastasis.

Authors

Institutions

Publication Details

Journal
Scientific Reports
Published
2025-04-27
DOI
https://doi.org/10.1038/s41598-025-99685-3
Citations
3
Primary Topic
Brain Metastases and Treatment
Type
article
Field-Weighted Citation Impact
4.56

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

GRB2 promotes brain metastasis in HER2-positive breast cancer by regulating the Ras/MAPK pathway

Dan Liu, Hongyu Li, Yalin Zhang, Xiao Han et al.
3 citations
Scientific Reports
Brain Metastases and Treatment
4.56
article

GRB2 promotes brain metastasis in HER2-positive breast cancer by regulating the Ras/MAPK pathway

Dan Liu, Hongyu Li, Yalin Zhang, Xiao Han, Bingyu Li, Gang Sun
article en
3 citations

Abstract

Brain metastasis is emerging as the most serious concern for breast cancer patients. HER2-positive breast cancer is more prone to undergo brain metastasis than other subtypes; notably, there has been little improvement in the treatment of brain metastasis .Our study confirmed the relevance of HER2 status to brain metastasis risk via clinical data analysis and revealed that exerts GRB2 tumorigenic effects by regulating the Ras/MAPK pathway in vivo and in vitro. Both an in situ injection model and a direct cerebral injection model were used to explore the ability of GRB2 to promote the brain metastasis. Results indicated that HER2- positive is a risk factor for brain metastasis according to clinical data. GRB2 enhances proliferation, migration, and invasion while suppressing apoptosis in HER2-positive breast cancer cells in vitro, primarily by regulating phosphorylation and alternative splicing of key proteins within the Ras/MAPK pathway. Notably, tumor cells were able to cross the blood‒brain barrier in both models assessed in this study. Thus, GRB2 is an oncogenic factor that contributes to the malignancy of HER2-positive breast cancer, GRB2 and HER2 can synergistically promote tumor cell penetration of the blood‒brain barrier and induce metastasis.

Scientific ReportsVol. 15(1)
Xinjiang Medical University (CN), Tumor Hospital of Xinjiang Medical University (CN)
Natural Science Foundation of Xinjiang
Good health and well-being
Openalex Percentile: Top 6%
Brain Metastases and Treatment
4.56
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.