GTPBP2 inactivates Hippo signaling to promote triple-negative breast cancer cell malignancy.

Breast cancer (BC) remains the leading cause of cancer-related mortality among women worldwide, with triple-negative breast cancer (TNBC) exhibiting the poorest prognosis. GTPBP2, a member of the G protein superfamily, has primarily been studied in the context of human genetics, with no reported research on its role in BC. This study aims to explore the effects of GTPBP2 on proliferation, migration, and invasion in TNBC, as well as to elucidate its underlying mechanisms. In this study, GTPBP2 expression was analyzed using multiple breast cancer-related databases. Western blotting was employed to validate the protein expression of GTPBP2 and its potential mechanisms in human breast cancer. Additionally, lentiviral infection was used to alter GTPBP2 expression in TNBC cells, and the effects on cancer cell proliferation, migration, and invasion were assessed in vitro using CCK-8 assays, colony formation assays, wound-healing assays, and Transwell invasion analyses. To further evaluate the role of GTPBP2 in vivo, xenograft tumors were established in female B-NDG mice to study tumor occurrence and progression. GTPBP2 is significantly upregulated in TNBC tissues and plays a critical role in promoting the malignant progression of breast cancer by positively regulating key pathways associated with tumor growth and metastasis.