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Updated: Aug 15, 2025

Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
Published on: June 7, 2016
Has_circ_0048764 promotes breast cancer progression by sponging miR-578 and regulating HMGA2 expression
Mingjian Ding1,2, Dianlu Dai2, Wenhua Yang2
1Breast Center, The Fourth Hospital of Hebei Medical University, Shijiangzhuang, Hebei, P.R. China.
Background:
Circular RNAs (circRNAs) function as important regulators in the progression of cancers. The role of circRNA_0048764 (circ_0048764) in the development of breast cancer (BC) remains inconclusive. This work investigates the biological function and molecular mechanism of circ_0048764 in BC.
Methods:
Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression levels of circ_0048764, microRNA-578 (miR-578) and high mobility group AT-hook 2 (HMGA2) mRNA. The viability of BC cells was examined by cell counting kit 8 (CCK-8) assay. Besides, cyclin D1, proliferating cell nuclear antigen (PCNA) and HMGA2 expression levels were detected by western blot. The migrative and invasive capability of BC cells were probed by transwell assay. The relationships between miR-578 and circ_0048764 or HMGA2 3'-UTR were validated by dual-luciferase reporter gene assay.
Results:
Circ_0048764 was highly expressed in BC tissues and cells, which was significantly associated with tumor size (≥2 cm), lymph node status (positive), and higher TNM stage of BC patients. Circ_0048764 depletion suppressed the proliferative, migrative, and invasive abilities of BC cells, which was rescued by transfection of miR-578 inhibitors. The binding sites were verified between circ_0048764 and miR-578. HMGA2 was identified to be a target of miR-578 in BC cells, and circ_0048764 positively regulated HMGA2 expression in BC cells via repressing miR-578.
Conclusion:
Circ_0048764 promotes BC cell growth, migration and invasion via absorbing miR-578 and up-regulating HMGA2.
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