SRPRB can regulate proliferation and migration in Triple-Negative breast cancer cells

Breast cancer is the leading cause of cancer-related deaths in women worldwide, and triple-negative breast cancer (TNBC), accounting for 15-20% of all breast cancer cases, has the poorest prognosis among all subtypes. As a component of the signal recognition particle (SRP) receptor (SR) complex, SRPRB is involved in tumorigenesis and progression, yet its specific regulatory mechanism in TNBC remains to be elucidated.

Bioinformatics analysis was used to detect SRPRB expression in TNBC, and its expression in TNBC cell lines was validated by qRT-PCR and Western blot. CCK-8 and colony formation assays were performed to evaluate the effect of SRPRB on tumor cell proliferation, while Transwell and wound healing assays were used to verify its roles in cell migration and invasion. Flow cytometry and Hoechst staining were applied to investigate the impact of SRPRB knockdown on TNBC cell apoptosis, and Western blot was used for protein expression detection.

Our findings demonstrated that SRPRB was highly expressed in tumor tissues of TNBC patients. Univariate and multivariate analyses revealed that high SRPRB expression was associated with poor overall survival (OS) and recurrence-free survival (RFS) in TNBC patients. In in vitro experiments, SRPRB was highly expressed in two TNBC cell lines, and SRPRB knockdown significantly inhibited the proliferation, migration and invasion of TNBC cells. Furthermore, SRPRB knockdown induced cell apoptosis, and subsequent Western blot assays confirmed that SRPRB knockdown suppressed the WNT signaling pathway.

SRPRB is a promising prognostic biomarker for TNBC. Knockdown of SRPRB can induce cell apoptosis, suppress cell proliferation and migration, and down regulate the expression of key regulatory proteins. These findings not only confirm the value of SRPRB as a clinically relevant prognostic indicator but also highlight its therapeutic potential as a molecular target for TNBC intervention strategies.