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Updated: Aug 4, 2025
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Network Pharmacology and Experimental Validation to Explore the Effect and Mechanism of Kanglaite Injection Against
Mei Zhao1,2, Lijuan Fu1,2, Panling Xu1,2
1Department of Chinese Integrative Medicine Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, People's Republic of China.
Purpose:
Kanglaite injection (KLTi), made of Coix seed oil, has been shown to be effective in the treatment of numerous cancers. However, the anticancer mechanism requires further exploration. This study aimed to investigate the underlying anticancer mechanisms of KLTi in triple-negative breast cancer (TNBC) cells.
Methods:
Public databases were searched for active compounds in KLTi, their potential targets and TNBC-related targets. KLTi's core targets and signaling pathways were determined through compound-target network, protein-protein interaction (PPI) network, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Molecular docking was carried out to predict the binding activity between active ingredients and key targets. In vitro experiments were conducted to further validate the predictions of network pharmacology.
Results:
Fourteen active components of KLTi were screened from the database. Fifty-three candidate therapeutic targets were selected, and bioinformatics analysis was performed to identify the top two active compounds and three core targets. GO and KEGG enrichment analyses indicated that KLTi exerts therapeutic effects on TNBC through the cell cycle pathway. Molecular docking results showed that the main compounds of KLTi exhibited good binding activity to key target proteins. Results from in vitro experiments showed that KLTi inhibited proliferation and migration of TNBC cell lines 231 and 468, induced apoptosis, blocked cells in the G2/M phase, downregulated the mRNA expression of seven G2/M phase-related genes cyclin-dependent kinase 1 (CDK1), cyclin-dependent kinase 2 (CDK2), and checkpoint kinase 1 (CHEK1), cell division cycle 25A (CDC25A), cell division cycle 25B (CDC25B), maternal embryonic leucine zipper kinase (MELK), and aurora kinase A (AURKA), as well as downregulated CDK1 protein expression and up-regulated protein expression of Phospho-CDK1.
Conclusion:
By utilizing network pharmacology, molecular docking, and in vitro experiments, KLTi was confirmed to have anti-TNBC effects by arresting cell cycle and inhibiting CDK1 dephosphorylation.
Insights
Kanglaite injection (KLTi) shows anti-triple-negative breast cancer (TNBC) effects by halting the cell cycle and inhibiting CDK1 dephosphorylation. This study explored KLTi
Area of Science:
- Oncology
- Pharmacology
- Bioinformatics
Background:
- Kanglaite injection (KLTi), derived from Coix seed oil, is recognized for its anticancer properties.
- The precise anticancer mechanisms of KLTi, particularly in triple-negative breast cancer (TNBC), warrant further investigation.
Purpose of the Study:
- To elucidate the underlying anticancer mechanisms of KLTi in triple-negative breast cancer (TNBC) cells.
- To validate the efficacy of KLTi against TNBC using a combination of network pharmacology, molecular docking, and in vitro assays.
Main Methods:
- Network pharmacology analysis of KLTi active components and TNBC targets.
- Protein-protein interaction (PPI) network construction and pathway enrichment analysis (GO and KEGG).
- Molecular docking simulations and in vitro validation in TNBC cell lines.
Main Results:
- Identification of key KLTi compounds and core targets involved in TNBC treatment.
- Enrichment analysis revealed the cell cycle pathway as a primary target of KLTi.
- In vitro studies confirmed KLTi's inhibition of TNBC cell proliferation, migration, and induction of apoptosis by arresting cells in the G2/M phase and modulating key cell cycle-related genes and proteins, including CDK1.
Conclusions:
- KLTi demonstrates significant anti-TNBC effects.
- The mechanism involves cell cycle arrest and inhibition of CDK1 dephosphorylation.
- This study provides a mechanistic basis for KLTi's application in TNBC therapy.
