LAUSR

Colorectal cancer (CRC) is the third frequent cancer and second leading reason of cancer‐related mortality all over the globe. Saponins from Platycodi radix (SPR) and microRNAs (miRNAs) have been reported to regulate CRC cell progression. Real‐time quantitative polymerase chain reaction (RT‐qPCR) detected miR‐181c‐5p, miR‐181d‐5p, and RBM47 expression level. Cell counting kit‐8 (CCK‐8), 5‐ethynyl‐20‐deoxyuridine (EdU), colony formation, transwell, and wound healing assays validated that miR‐181c‐5p and miR‐181d‐5p promote CRC cell proliferation, migration and invasion and SPR exerts opposite effects. Cignal Finder Reporter Array and western blot proved that the activity of PI3K/AKT pathway was decreased by RBM47 overexpression. RNA pulldown, luciferase reporter, and RNA‐binding protein immunoprecipitation (RIP) assays proved the interaction between miR‐181c/d‐5p and RBM47, and RBM47 and PTEN. Rescue experiments were carried out to validate that RBM47 reverses the influence of miR‐181c/d‐5p on the progression of CRC cells. The stability of PTEN was probed by real‐time quantitative polymerase chain reaction in CRC cells treated with Actinomycin D (Act D). To be concluded, SPR inactivates PI3K/AKT signaling pathway to suppress CRC cell proliferation, invasion, and migration via miR‐181c/d‐5p/RBM47. Elucidating the mechanisms of SPR underlying CRC may offer novel insight into CRC treatment.