circPOLA2 promotes proliferation, invasion, migration, and epithelial-mesenchymal transition in breast cancer via the miR-1224–5p/ HMGA2 axis

Objective: This study aimed to investigate the carcinogenic role of circPOLA2 in Breast Cancer (BC) and reveal its potential mechanism as a competitive endogenous RNA. Methods: Differentially expressed circRNAs, miRNAs, and mRNAs in BC tissues and cell lines were screened and analyzed by RT-qPCR. Th...

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Detalles Bibliográficos
Autores: Xu, XinYan, Li, Jie, Li, RuiJuan, Tan, YanFang, Lu, Zhibing
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:Brasil
Institución:Universidade de São Paulo (USP)
Repositorio:Clinics
Idioma:inglés
OAI Identifier:oai:revistas.usp.br:article/238763
Acceso en línea:https://revistas.usp.br/clinics/article/view/238763
Access Level:acceso abierto
Palabra clave:circPOLA2 miR-1224–5p HMGA2 Breast
Cancer Epithelial-Mesenchymal Transition
Metastasis
Descripción
Sumario:Objective: This study aimed to investigate the carcinogenic role of circPOLA2 in Breast Cancer (BC) and reveal its potential mechanism as a competitive endogenous RNA. Methods: Differentially expressed circRNAs, miRNAs, and mRNAs in BC tissues and cell lines were screened and analyzed by RT-qPCR. The interaction among circPOLA2, miR-1224–5p, and HMGA2 was tested using dual luciferase reporter assay and RNA pull-down assay. Cell proliferation was detected by MTT and colony formation assay, apoptosis was detected by flow cytometry, migration, and invasion was detected by Transwell assay, and EMT-related proteins were detected by Western blot. Results: circPOLA2 and HMGA2 levels were elevated in BC, while miR-1224–5p level was reduced. Knocking down circPOLA2 decreased the expression of HMGA2 by elevating miR-1224–5p expression. Knocking down circPOLA2 or HMGA2 or elevating miR-1224–5p reduced the proliferative, migratory, invasive, and antiapoptotic capacities of BC cells. Conclusion: Knockdown of circPOLA2 inhibits BC cell proliferation, migration, and invasion and delays BC tumor progression by regulating the miR-1224–5p/HMGA2 axis, providing a new strategy and target for therapeutic intervention in BC.