Frontiers in bioscience (Landmark edition) · 2026
RNA-Binding Protein RBMS3 Inhibits Cervical Cancer Progression by Enhancing HSPA6 mRNA Stability.
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Huang Huaping, Li Ping, Zhu Lixia, Wu Yawei, Liu Qin, Zhang Hong
Аннотация
BACKGROUND: Cervical cancer (CC) is a prevalent malignancy in women. RNA-binding motif single-stranded interacting protein 3 (RBMS3) acts as a tumor suppressor in many cancer types, but its role and underlying regulatory mechanisms in CC remain unclear.
METHODS: The expression levels of RBMS3 and heat shock protein family A member 6 (HSPA6) were evaluated in clinical CC tissues. Gain- and loss-of-function assays, transcriptome sequencing, and rescue experiments were performed in CC cell lines and nude mouse xenograft models.
RESULTS: RBMS3 expression was notably lower in CC tissues (n = 306) than in normal cervical tissues (n = 22), with reduced levels linked to shorter overall patient survival (p < 0.05). Overexpression of RBMS3 reduced cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo (p < 0.001). HSPA6 was identified as a key target of RBMS3 and was also downregulated in CC tissues. RBMS3 potentially binds to HSPA6 mRNA and enhances its stability. Knockdown of HSPA6 reversed the tumor-suppressive effects of RBMS3 (p < 0.001).
CONCLUSIONS: RBMS3 inhibits CC progression by stabilizing HSPA6 mRNA. The RBMS3-HSPA6 axis may represent a prognostic biomarker and therapeutic target in CC.
METHODS: The expression levels of RBMS3 and heat shock protein family A member 6 (HSPA6) were evaluated in clinical CC tissues. Gain- and loss-of-function assays, transcriptome sequencing, and rescue experiments were performed in CC cell lines and nude mouse xenograft models.
RESULTS: RBMS3 expression was notably lower in CC tissues (n = 306) than in normal cervical tissues (n = 22), with reduced levels linked to shorter overall patient survival (p < 0.05). Overexpression of RBMS3 reduced cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo (p < 0.001). HSPA6 was identified as a key target of RBMS3 and was also downregulated in CC tissues. RBMS3 potentially binds to HSPA6 mRNA and enhances its stability. Knockdown of HSPA6 reversed the tumor-suppressive effects of RBMS3 (p < 0.001).
CONCLUSIONS: RBMS3 inhibits CC progression by stabilizing HSPA6 mRNA. The RBMS3-HSPA6 axis may represent a prognostic biomarker and therapeutic target in CC.