Emerging roles for SNRPB2 in governing the cell cycle and steering tumor immune modulation in breast cancer.
Breast cancer is a common malignant tumor with limited treatment options and poor prognosis. SNRPB2, a core spliceosomal component involved in pre-mRNA splicing, is dysregulated in multiple cancers, but its role in breast cancer remains incompletely understood.
We analyzed SNRPB2 expression in breast cancer using TCGA, CPTAC, and HPA databases, and assessed its prognostic value via Kaplan-Meier plotter. The biological function of SNRPB2 was evaluated through in vitro cell line assay, and the underlying molecular mechanisms were determined via RNA-seq, RT-qPCR, and additional GEO datasets. Our findings demonstrated that SNRPB2 was significantly overexpressed in breast cancer tissues and correlated with malignant progression and poor prognosis. Knockdown of SNRPB2 induced G2/M cell cycle arrest in cancer cells, decreased expression of numerous genes related to cell cycle and immune modulation, and triggered alterations in multiple alternative splicing events. Mechanistically, SNRPB2 knockdown might promote cancer cell cycle arrest by regulating HMGA2 splicing and expression, while simultaneously suppressing the expression of immune-related genes such as CSF1, CSF1R, IL6, and CX3CL1. Immune infiltration analysis revealed that SNRPB2 expression correlated with increased infiltration of activated inflammatory cells and myeloid-derived suppressor cells.
SNRPB2 potentially plays a dual role in promoting breast cancer progression and shaping the immunosuppressive microenvironment, partly through HMGA2 splicing modulation and immune-regulatory gene suppression. These findings suggest that SNRPB2 may represent a promising therapeutic target for breast cancer.
We analyzed SNRPB2 expression in breast cancer using TCGA, CPTAC, and HPA databases, and assessed its prognostic value via Kaplan-Meier plotter. The biological function of SNRPB2 was evaluated through in vitro cell line assay, and the underlying molecular mechanisms were determined via RNA-seq, RT-qPCR, and additional GEO datasets. Our findings demonstrated that SNRPB2 was significantly overexpressed in breast cancer tissues and correlated with malignant progression and poor prognosis. Knockdown of SNRPB2 induced G2/M cell cycle arrest in cancer cells, decreased expression of numerous genes related to cell cycle and immune modulation, and triggered alterations in multiple alternative splicing events. Mechanistically, SNRPB2 knockdown might promote cancer cell cycle arrest by regulating HMGA2 splicing and expression, while simultaneously suppressing the expression of immune-related genes such as CSF1, CSF1R, IL6, and CX3CL1. Immune infiltration analysis revealed that SNRPB2 expression correlated with increased infiltration of activated inflammatory cells and myeloid-derived suppressor cells.
SNRPB2 potentially plays a dual role in promoting breast cancer progression and shaping the immunosuppressive microenvironment, partly through HMGA2 splicing modulation and immune-regulatory gene suppression. These findings suggest that SNRPB2 may represent a promising therapeutic target for breast cancer.