Research Paper Volume 16, Issue 3 pp 2848—2865

Mechanism of Erianin anti-triple negative breast cancer based on transcriptomics methods and network pharmacology

Ming Li1, , Yuan Zhao2, , Huimin Li1, , Shiyao Kang1, , Xuming Deng1, , Miaomiao Sheng1, ,

  • 1 Laboratory of Molecular Genetics of Aging and Tumour, Medical School, Kunming University of Science and Technology, Chenggong Campus, Kunming, Yunnan 650500, China
  • 2 Kunming University of Science and Technology Affiliated Puer City People’s Hospital, Puer, Yunnan 665000, China

Received: September 4, 2023       Accepted: December 13, 2023       Published: February 7, 2024
How to Cite

Copyright: © 2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Triple negative breast cancer (TNBC) is a highly aggressive illness that lacks effective targeted treatments. Although Erianin has shown potential antitumor properties, its precise mechanism of action and target in TNBC remain unclear, hampering the development of drugs. The present study investigated the underlying mechanism of action of Erianin in treating TNBC by using transcriptomics and network pharmacology approaches. We evaluated Erianin’s bioactivity in TNBC cell lines and xenograft tumor models. The results showed that Erianin significantly inhibited TNBC cell proliferation and impeded tumor growth. A subsequent analysis of transcriptomic and network pharmacological data identified 51 mutual targets. Analysis of protein-protein interactions identified eight hub targets. Furthermore, molecular docking indicated that the PPARA binding energy was the lowest for Erianin among the hub targets, followed by ROCK2, PDGFRB, CCND1, MUC1, and CDK1. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis showed that the common targets were associated with multiple cancer-related signaling pathways, including focal adhesion, PI3K-Akt signaling pathway, Rap1 signaling pathway, microRNAs in cancer, and human papillomavirus infection. The results of the Western blot and immunohistochemistry experiment further showed that Erianin could suppress PI3K/Akt signaling pathway activation. After co-incubation with SC79, the cell inhibition rate of Erianin was decreased, which further confirmed that Erianin inhibits TNBC progression via the PI3K-AKT signaling pathway. In conclusion, our results indicated that Erianin has the potential to inhibit the proliferation of TNBC by downregulating the PI3K/AKT signaling pathway by transcriptomics and network pharmacology. Therefore, Erianin appears to be a promising compound for the effective treatment of TNBC.


BC: Breast cancer; ER: Estrogen receptor; PR: Progesterone receptor; HER2: Human epidermal growth factor receptor 2; TNBC: Triple negative breast cancer; DEGs: Differentially expressed genes; BPs: Biological processes; CCs: Cellular localisations; MFs: Molecular functions; WB: Western blot; IHC: Immunohistochemistry; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; DMEM: Dulbecco’s modified Eagle’s medium; OD: Optical density; CCK-8: Cell Counting Kit-8; CCND1: Cyclin D1; APOE: Apolipoprotein E; PDGFRB: Platelet-derived growth factor receptor-beta; PLAU: Plasminogen Activator, Urokinase; CDK1: Cyclin Dependent Kinase 1; PPARA: Peroxisome proliferator-activated receptor alpha; ROCK2: Rho Associated Coiled-Coil Containing Protein Kinase 2; MUC1: Mucin1.