Circ_0000395 Promoted CRC Progression via Elevating MYH9 Expression by Sequestering miR-432-5p
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Updated: Sep 6, 2025

Detection of a Circulating MicroRNA Custom Panel in Patients with Metastatic Colorectal Cancer
Published on: March 14, 2019
Leilei Fan1, Weiwei Li1, Hongsheng Jiang2
1Department of Gastrointestinal Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, No.158 Wuyang Avenue, Enshi City, Hubei Province, China.
Abstract:
Colorectal cancer (CRC) has been listed as the fourth deadly cancer. Circular RNA hsa_circRNA_001046, also termed as hsa_circ_0000395 (circ_0000395), has been shown to be upregulated in CRC. Nevertheless, the function of circ_0000395 in CRC progression is unclear. 42 CRC patients were enrolled in the study. Detection of circ_0000395 expression in tissues and cells was executed using real-time quantitative polymerase chain reaction (RT-qPCR). Evaluation of circ_0000395 function was performed using loss-of-function experiments in vitro and in vivo. The regulatory mechanism of circ_0000395 was predicted by bioinformatics analysis and validated by dual-luciferase reporter and RIP assays. Exosomes were isolated by ultracentrifugation and validated by western blotting, TEM, and NTA. Circ_0000395 was strongly expressed in CRC samples and cell lines. Also, circ_0000395 repressed CRC growth in mouse models in vivo and induced CRC cell apoptosis, restrained CRC cell proliferation, migration, invasion, and EMT in vitro. Mechanistically, circ_0000395 sequestered miR-432-5p to regulate MYH9 expression. Furthermore, miR-432-5p knockdown reversed circ_0000395 silencing-mediated effects on CRC cell malignant phenotypes. MYH9 overexpression counteracted the inhibiting effects of miR-432-5p upregulation on CRC cell malignant phenotypes. Additionally, CRC cells derived from exosomal circ_0000395 promoted cancer cell malignant phenotypes. Our findings demonstrated that circ_0000395 sequestered miR-432-5p to elevate MYH9 expression, resulting in facilitating CRC progression, manifesting a potential therapeutic target for CRC.
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