The Expression and Clinical Value of <scp>miR</scp> ‐483‐5p in Cervical Cancer and Its Regulation of Cervical Cancer via <scp>TIMP2</scp>

BACKGROUND: Cervical cancer (CC) is a major public health issue threatening women's health, and its early diagnosis and prognosis evaluation are very important. miR-483-5p has been identified as an oncogene in multiple cancers, but its molecular mechanism in CC is still unclear. OBJECTIVE: This study aims to explore the biological functions and regulatory mechanisms of miR-483-5p in CC. METHODS: miR-483-5p expression levels in CC were detected by qRT-PCR. The prognostic value of miR-483-5p was established via Kaplan-Meier survival analysis and Cox regression analysis. CCK-8 and Transwell assays served to analyze its regulatory effects on CC cell proliferation, migration, and invasion. Dual luciferase reporter assay validated the targeted binding relationship between miR-483-5p and TIMP2. Co-inhibition assays investigated the molecular mechanism of miR-483-5p in CC. RESULTS: miR-483-5p is significantly increased in CC (p < 0.001) and correlates with LNM, differentiation, tumor size, and FIGO stage. Elevated miR-483-5p was an independent factor of poor survival in CC (HR = 9.942, 95% CI = 4.395-22.488). miR-483-5p inhibitors significantly suppressed CC cell malignant progression. TIMP2 as a direct target of miR-483-5p. miR-483-5p accelerated CC development by inhibiting TIMP2. CONCLUSIONS: miR-483-5p is significantly overexpressed in CC and functions as an oncogene by directly targeting and suppressing TIMP2 expression, thereby promoting cancer cell malignant progression.