Prognostic value and cellular function of hsa_circ_0001588 in breast cancer.
OpenAlex 토픽 ·
Circular RNAs in diseases
Cancer Mechanisms and Therapy
Wnt/β-catenin signaling in development and cancer
[BACKGROUND] As a frequently occurring malignant disorder in women, breast cancer (BC) is closely associated with circular RNAs (circRNAs) in mediating its pathological progression.
APA
Wei Wu, Zichen Gao, et al. (2026). Prognostic value and cellular function of hsa_circ_0001588 in breast cancer.. Cytotechnology, 78(3), 81. https://doi.org/10.1007/s10616-026-00920-0
MLA
Wei Wu, et al.. "Prognostic value and cellular function of hsa_circ_0001588 in breast cancer.." Cytotechnology, vol. 78, no. 3, 2026, pp. 81.
PMID
41953107
Abstract
[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 .
[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 . Rescue strategies involving miR-525-3p inhibition or 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 . The inhibitory effects resulting from the knockdown of hsa_circ_0001588 can be reversed by either inhibiting miR-525-3p or overexpressing .
[CONCLUSIONS] Hsa_circ_0001588 emerges as a critical regulator of BC malignancy by modulating the miR-525-3p/ 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.
[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 .
[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 . Rescue strategies involving miR-525-3p inhibition or 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 . The inhibitory effects resulting from the knockdown of hsa_circ_0001588 can be reversed by either inhibiting miR-525-3p or overexpressing .
[CONCLUSIONS] Hsa_circ_0001588 emerges as a critical regulator of BC malignancy by modulating the miR-525-3p/ 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.
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