Cell Metabolomics Reveals the Potential Mechanism of Aloe Emodin and Emodin Inhibiting Breast Cancer Metastasis

• Published in: International journal of molecular sciences Vol. 23; no. 22; p. 13738
• Main Authors: Cheng, Guorong, Liu, Zhiqiang, Zheng, Zhong, Song, Fengrui, Zhuang, Xiaoyu, Liu, Shu
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 08.11.2022; MDPI
• Subjects: Aloe; aloe emodin (AE); Angiogenesis; Anoikis; Anthraquinones - pharmacology; Biomarkers; Biosynthesis; Breast cancer; Cell culture; cell metabolomics; Colorectal cancer; Cytotoxicity; Drug resistance; Emodin; emodin (EMD); Emodin - pharmacology; Homocysteine; Humans; Melanoma, Cutaneous Malignant; Metabolism; Metabolites; Metabolomics; Metastases; Metastasis; Methionine; Multivariate statistical analysis; Neoplasms, Second Primary; Phenotypes; Polyamines; Quantitative analysis; Statistical analysis; Tricarboxylic acid cycle; Tumors; breast cancer; cell metabolomics; metastasis; aloe emodin (AE); emodin (EMD)
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms232213738

Metastasis is one of the main obstacles for the treatment and prognosis of breast cancer. In this study, the effects and possible mechanisms of aloe emodin (AE) and emodin (EMD) for inhibiting breast cancer metastasis were investigated via cell metabolomics. First, a co-culture model of MCF-7 and HUVEC cells was established and compared with a traditional single culture of MCF-7 cells. The results showed that HUVEC cells could promote the development of cancer cells to a malignant phenotype. Moreover, AE and EMD could inhibit adhesion, invasion, and angiogenesis and induce anoikis of MCF-7 cells in co-culture model. Then, the potential mechanisms behind AE and EMD inhibition of MCF-7 cell metastasis were explored using a metabolomics method based on UPLC-Q-TOF/MS multivariate statistical analysis. Consequently, 27 and 13 biomarkers were identified in AE and EMD groups, respectively, including polyamine metabolism, methionine cycle, TCA cycle, glutathione metabolism, purine metabolism, and aspartate synthesis. The typical metabolites were quantitatively analyzed, and the results showed that the inhibitory effect of AE was significantly better than EMD. All results confirmed that AE and EMD could inhibit metastasis of breast cancer cells through different pathways. Our study provides an overall view of the underlying mechanisms of AE and EMD against breast cancer metastasis.