The Expression and Clinical Value of miR-483-5p in Cervical Cancer and Its Regulation of Cervical Cancer via TIMP2

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.

This study aims to explore the biological functions and regulatory mechanisms of miR-483-5p in CC.

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.

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.

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.