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Updated: Oct 20, 2025

In Silico Identification and Characterization of circRNAs During Host-Pathogen Interactions
Published on: October 21, 2022
Circular RNA circ_0089153 acts as a competing endogenous RNA to regulate colorectal cancer development by the
Guan Fang1, Tingting Chen2, Ruibo Mao1
1Department of Colorectal and Anal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Abstract:
Increasing evidence has indicated the implications of circular RNAs (circRNAs) in the development of colorectal cancer (CRC). In this study, we investigated the functional role and mechanism of circ_0089153 in CRC pathogenesis. The expression levels of circ_0089153, microRNA (miR)-198, and SUMO-specific peptidase 1 (SENP1) were gauged by quantitative real-time PCR (qRT-PCR) or western blot. Cell proliferation, sphere formation, tube formation, and apoptosis abilities were detected by 5-Ethynyl-2'-Deoxyuridine (EdU), sphere formation, tube formation, and flow cytometry assays, respectively. The direct relationship between miR-198 and circ_0089153 or SENP1 was verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The mouse xenograft assays were performed to evaluate the role of circ_0089153 in vivo. Our data showed that circ_0089153 was overexpressed in CRC tissues and cells. Depletion of circ_0089153 repressed cell proliferation, sphere formation ability, and enhanced cell apoptosis, as well as inhibited tube formation in vitro. Moreover, circ_0089153 depletion diminished tumor growth in vivo. Mechanistically, circ_0089153 targeted miR-198, and the effects of circ_0089153 were mediated by miR-198. SENP1 was identified as a direct and functional target of miR-198. Circ_0089153 worked as a competing endogenous RNA (ceRNA) to post-transcriptionally regulate SENP1 expression by miR-198. Our findings identify circ_0089153 as a novel regulator of CRC development through the regulation of the miR-198/SENP1 axis and establish a strong rationale for developing circ_0089153 as a promising therapeutic against CRC.
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