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Updated: Jun 23, 2025

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
CircACTR2 promotes bladder cancer progression through IKBKB-mediated NF-κB signaling pathway activation
Ping Li1, Zhang Zhao2, Qichao Chen3
1Department of Urology Surgery, Jinling Hospital, Jinling School of Clinical Medicine, Nanjing Medical University, Nanjing, 210001, Jiangsu, China.
Background:
Circular RNAs (circRNAs) have significant roles in tumor progression. The role of circRNA derived from ARP2 actin-related protein 2 homolog (circACTR2) has been reported in various human diseases. However, the functions and regulatory mechanisms of circACTR2 in Bladder Cancer (BCa) remain unknown.
Objectives:
This study aims to explore the biological role and regulatory mechanism of circACTR2 in BCa.
Methods:
We analyzed the effects of circACTR2 on BCa through bioinformatics analyses, RT-qPCR, and cell function assays.
Results:
We observed the upregulation of circACTR2 in BCa tissues and validated its circular structure. Loss-of-function assays demonstrated that silencing circACTR2 suppressed the proliferation, invasion, and migration of BCa cells. Mechanistic investigation revealed that circACTR2 sponges miR-219a-2-3p to elevate the expression of the inhibitor of nuclear factor kappa B kinase subunit beta (IKBKB). This induced upregulation of IKKβ protein promoted the nuclear translocation of p65, thereby activating the NF-κB signaling pathway.
Conclusions:
Our findings indicate that circACTR2 promotes BCa cell proliferation, migration, and invasion by activating the NF-κB signaling pathway via the miR-219a-2-3p/IKBKB axis, potentially unveiling a new therapeutic target for BCa.
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