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Detection of a Circulating MicroRNA Custom Panel in Patients with Metastatic Colorectal Cancer
Published on: March 14, 2019
Prognostic value and cellular function of hsa_circ_0001588 in breast cancer
Wei Wu1, Zichen Gao2, Sijing Gao3
1Breast and Thyroid Surgery, Dazhou Central Hospital, Dazhou, 635000 China.
Background:
As a frequently occurring malignant disorder in women, breast cancer (BC) is closely associated with circular RNAs (circRNAs) in mediating its pathological progression. Accumulating evidence suggests that hsa_circ_0001588 promotes BC via microRNA (miRNA) sponging.
Aim:
To investigate the expression dynamics, functional contributions, and molecular underpinnings of hsa_circ_0001588 in BC progression, focusing on its regulatory axis with miR-525-3p and KPNB1.
Methods:
Clinical BC tissues and cell lines were used to validate hsa_circ_0001588 expression via RT-qPCR. Cell proliferation was evaluated via MTT assay, whereas migration and invasion capacities were assessed using Transwell systems. Dual-luciferase reporter assays and RIP were implemented to validate the reciprocal interactions among hsa_circ_0001588, miR-525-3p, and KPNB1. Rescue strategies involving miR-525-3p inhibition or KPNB1 overexpression were thereafter executed to validate the regulatory axis.
Results:
Hsa_circ_0001588 exhibited elevated expression in BC tissues and cell lines, demonstrating positive associations with advanced TNM staging and unfavorable prognosis. Depletion of hsa_circ_0001588 impaired proliferative, migratory, and invasive capacities, as well as EMT in cells. Mechanistically, hsa_circ_0001588 directly binds to miR-525-3p, relieving its repression on KPNB1. The inhibitory effects resulting from the knockdown of hsa_circ_0001588 can be reversed by either inhibiting miR-525-3p or overexpressing KPNB1.
Conclusions:
Hsa_circ_0001588 emerges as a critical regulator of BC malignancy by modulating the miR-525-3p/KPNB1 axis. Its overexpression correlates with poor prognosis, positioning it as a promising diagnostic marker and actionable therapeutic target.
Supplementary Information:
The online version contains supplementary material available at 10.1007/s10616-026-00920-0.
