Long Noncoding RNA TOB1‐AS1 Represses Cervical Cancer Cell Proliferation, Invasion, and Migration via the MicroRNA‐27a‐3p/Thioredoxin‐Interacting Protein Molecular Axis

ABSTRACT

Cervical cancer (CC) remains a major global health concern, particularly due to its aggressive nature and limited treatment options in advanced stages. Long noncoding RNA (lncRNA) TOB1‐AS1 has been proposed as a tumor suppressor, yet its regulatory mechanism in CC remains unclear. This study aimed to elucidate the role of TOB1‐AS1 in CC progression through the miR‐27a‐3p/thioredoxin‐interacting protein (TXNIP) molecular axis. Functional gain‐ and loss‐of‐function assays were conducted to assess the effects of TOB1‐AS1, miR‐27a‐3p, and TXNIP on cell proliferation, invasion, migration, and apoptosis. RT‐qPCR, Western blotting, dual‐luciferase reporter assays, and in vivo xenograft models were used to validate interactions and phenotypic outcomes. TOB1‐AS1 was found to be downregulated in CC cells. Its overexpression suppressed proliferation, invasion, and migration, while enhancing apoptosis. Mechanistically, TOB1‐AS1 functioned as a competing endogenous RNA (ceRNA) by sponging miR‐27a‐3p, thereby restoring TXNIP expression. Modulating miR‐27a‐3p or TXNIP levels partially reversed the effects of TOB1‐AS1. In vivo, TOB1‐AS1 overexpression significantly inhibited tumor growth and altered miR‐27a‐3p and TXNIP expression profiles. These findings suggest that lncRNA TOB1‐AS1 acted as a ceRNA of miR‐27a‐3p to upregulate TXNIP, thereby suppressing CC cell proliferation, invasion and migration.