CircFAM120B promotes prostate cancer progression through miR-1182 inhibition and FBXO17-mediated AKT activation.

Circular RNAs (circRNAs) have emerged as key post-transcriptional regulators in cancer progression through their ability to modulate microRNA (miRNA) activity. However, the functional role and regulatory mechanisms of many circRNAs in prostate cancer (PCa) remain poorly understood. This study investigates the oncogenic potential of circFAM120B (hsa_circ_0001666) and its regulatory interaction with miR-1182 and FBXO17 in PCa. CircFAM120B expression was assessed in PCa tissues and cell lines using qRT-PCR and confirmed by Sanger sequencing and RNase R digestion. Functional assays, including CCK-8, EdU, colony formation, wound healing, Transwell, and flow cytometry, were performed to evaluate the effects of circFAM120B knockdown. RNA pull-down, dual-luciferase reporter, and rescue assays were conducted to investigate the molecular interaction between circFAM120B, miR-1182, and FBXO17. Additionally, a xenograft tumor model was used to validate in vivo tumorigenic effects. CircFAM120B was significantly upregulated in PCa tissues and cells and exhibited high cytoplasmic stability. Knockdown of circFAM120B suppressed PCa cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) while promoting apoptosis. Mechanistically, circFAM120B functioned as a sponge for miR-1182, thereby relieving its suppression of FBXO17. This axis led to activation of the AKT signaling pathway, which was attenuated following circFAM120B knockdown. Rescue experiments with a miR-1182 inhibitor confirmed that circFAM120B exerts its oncogenic effects via the miR-1182/FBXO17/AKT axis. In vivo, circFAM120B knockdown reduced tumor growth and metastatic potential in a PCa xenograft model. CircFAM120B promotes PCa progression by sponging miR-1182 and upregulating FBXO17 expression. Targeting the circFAM120B/miR-1182/FBXO17 axis may represent a novel therapeutic strategy for PCa. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-025-04677-9.