Anti-lung cancer effect of Ornithogalum caudatum Jacq. via the CRHBP and regulation of M2 macrophage polarization

Abstract Objectives This study aimed to validate OCJ’s anti-lung cancer effect and CRHBP regulation mechanism in vitro . Methods The ETCM database was searched to identify the main components and specific targets of OCJ. According to the HPA database, the immunohistochemical (IHC) images of normal lung cells and lung cancer cells were screened. The CCK-8 assay and flow cytometry were employed to evaluate the impact of OCJ on cancer cell viability, proliferation, and apoptosis before and following CRHBP knockout. Finally, the mechanisms by which OCJ regulates M2 macrophages were explored. Results The major component of OCJ was Caudaside A, and the specific target was CRHBP, according to the ETCM database. CRHBP was found to be expressed at a lower level in lung cancer tissue and cells compared to normal tissue and cells. However, the expression level of CRHBP was increased by the addition of OCJ. In the cell functional assay, OCJ failed to effectively suppress cell proliferation or induce cell apoptosis following CRHBP knockdown. The inhibitory effects of OCJ on the M2 polarization markers of macrophages rescued by CRHBP suppression. Conclusions OCJ can promote the overexpression of CRHBP to inhibit the polarization of M2 macrophages, thus inhibiting lung cancer cell proliferation and inducing apoptosis.