Cancercellresearch 2025, 12(46), 1021-1025;
https://doi.org/10.54762_ccr2025.48.1021-1025 (registering DOI)
- 13 Apr. 26
Abstract
Breast cancer remains the most common malignancy in women worldwide and continues to impose a substantial burden in terms of incidence and mortality. Ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation and reactive oxygen species accumulation, has emerged as an important process in tumor biology and a potential target for cancer therapy.
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Abstract: Breast cancer remains the most common malignancy in women worldwide and continues to impose a substantial burden in terms of incidence and mortality. Ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation and reactive oxygen species accumulation, has emerged as an important process in tumor biology and a potential target for cancer therapy. G protein subunit beta 2 (GNB2) has recently been implicated in several human malignancies; however, its role in breast cancer and the underlying mechanism remain poorly defined. In this study, we investigated the expression, biological function and mechanistic relevance of GNB2 in breast cancer. Co-immunoprecipitation, qPCR, western blotting, flow cytometry and biochemical assays were used to define the role of GNB2 in breast cancer cells. GNB2 was found to be upregulated in breast cancer and to promote malignant progression. Mechanistically, GNB2 interacted with HSPA5 and suppressed ferroptosis by increasing HSPA5 expression, thereby enhancing the proliferative and migratory capacity of breast cancer cells. Together, these findings identify GNB2 as a promoter of breast cancer progression and suggest that its oncogenic effects are mediated, at least in part, through HSPA5-dependent inhibition of ferroptosis. Our study highlights the GNB2-HSPA5 axis as a biologically relevant pathway in breast cancer and a potential target for further therapeutic investigation.
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(This article belongs to the Section Cancer cell Research)