Cell metabolomics identify regulatory pathways and targets of magnoline against prostate cancer

Abstract

Prostate cancer is known as a common malignant tumor in clinics and moreover, traditional chemotherapeutic drugs have great toxic side effects and drug resistance. Therefore, the searching the highly efficient and low toxicity antitumor drugs from natural drugs has become an important approach for the treatment of prostate cancer. Many studies showed that Cortex Phellodendri has important therapeutic significance for prostate cancer. Magnoline is the main component of Cortex Phellodendri Amurensis, and it is of great significance to evaluate the effect of magnoline on prostate cancer. By using metabolomics, we established a comprehensive analysis strategy based on cell metabolic analysis to study the inhibitory effect of magnoline on the proliferation of prostate cancer cell line 22RV1, and finally conducted an analysis on the cell metabolism footprint samples. Results showed that magnoline had a significant inhibitory effect on the proliferation of the prostate cancer cell line 22RV1. According to the established cell metabolomics methods, we found that 12 metabolic biomarkers of the cell metabolic footprint samples, respectively, could inhibit the proliferation of prostate cancer cells. Magnoline could significantly affect these metabolic biomarkers to disrupt the growth and proliferation of the prostate cancer cell line 22RV1. Additionally, through MetPA analysis indicated that these biomarkers were closely correlated with a variety of metabolic pathways in tumor cells, including the energy metabolism, amino acid metabolism and fatty acid metabolism, most of which were associated with nutrition and energy metabolism. Therefore, we speculated that because of the disturbance of nutrition metabolism and energy metabolism of the prostate cancer cell line 22RV1, cells could not provide the material basis for rapid proliferation, eventually resulting in the inhibition effect.

Keywords: Magnoline; Metabolomics; Prostatic cancer; Regulatory pathways; Targets.