Astragaloside IV regulates circ_0001615 and miR‐873‐5p/LASP1 axis to suppress colorectal cancer cell progression

Abstract Astragaloside IV (AS‐IV) has exhibited pivotal anti‐cancer efficacy in multiple types of cancer, including colorectal cancer (CRC). Meanwhile, circular RNA (circRNA) circ_0001615 has been reported to be involved in the malignant development of CRC. Herein, this study is expected to figure out the interaction between circ_0001615 and AS‐IV on CRC progression. The 50% inhibition concentration (IC50), proliferation, apoptosis, and migration were detected by Cell Counting Kit‐8 (CCK‐8), 5‐ethynyl‐2′‐deoxyuridine (EdU), flow cytometry, and wound healing assays. The expression of related proteins was examined by western blot. Circ_0001615, microRNA‐873‐5p (miR‐873‐5p), and LIM and SH3 protein 1 (LASP1) levels were detected by real‐time quantitative polymerase chain reaction (RT‐qPCR). The binding between miR‐873‐5p and circ_0001615, or LASP1, was predicted by Starbase, followed by verification by dual‐luciferase reporter and RNA immunoprecipitation (RIP) assays. The biological role of circ_0001615 and AS‐IV on CRC tumor growth was detected by the xenograft tumor model in vivo. According to the IC50 of AS‐IV in CRC cells, the 100 ng/mL AS‐IV treatment for 24 h was chosen for the following research: Our data confirmed that AS‐IV is a beneficial anti‐cancer agent in CRC cells. Furthermore, circ_0001615 and LASP1 expression were increased, and miR‐873‐5p was decreased in CRC patients and cell lines, whereas their expression exhibited an opposite trend in AS‐IV‐treated cells. Functionally, applying AS‐IV might act as a beneficial anti‐cancer effect by downregulating circ_0001615 in CRC cells in vitro. Mechanically, circ_0001615 serves as a sponge for miR‐873‐5p to affect LASP1 expression. In addition, AS‐IV inhibited CRC cell growth in vivo by modulating circ_0001615. Overall, AS‐IV could mitigate CRC development, at least in part, through the circ_0001615/miR‐873‐5p/LASP1 axis. These findings support a theoretical basis for an in‐depth study of the function of AS‐IV and the clinical treatment of CRC.