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Identification of small compounds targeting ferroptosis in triple-negative breast cancer by using an integrated
Mingzhen Qin1, Maoyuan Zhu2, Yifei Chen2
1Department of Biochemistry and Molecular Biology, College of Basic Medicine, Guangxi Medical University, 22 Shuangyong Road, Nanning, China; National Engineering Research Center of Southwest Endangered Medicinal Resources Development, Guangxi Botanical Garden of Medicinal Plants, 189 Changgang Road, Nanning, China.
Abstract:
This study integrated bioinformatics and computational approaches to identify potential therapeutic compounds targeting ferroptosis in triple-negative breast cancer (TNBC) patients. Through analysis of TNBC transcriptomic data from the GEO and FerrDb databases, we identified 140 TNBC-associated ferroptosis genes. There were seven hub genes (KRAS, PKM, MAPK1, AR, AURKA, TFRC and ESR1), which emerged as potential diagnostic biomarkers. Using computational screening and ADME analysis, we found four bioactive compounds (DHEA, cinnamaldehyde, glycyrrhetin and shikonin) that targeted MAPK1. Molecular docking and dynamics simulations further validated three optimal candidates (DHEA, glycyrrhetin and shikonin) with strong binding affinity to MAPK1. These findings suggest that targeting MAPK1-mediated ferroptosis may represent a promising therapeutic strategy for the treatment of TNBC patients. This study provides new insights into ferroptosis regulation in TNBC and it identified potential compounds for further drug development.
Insights
Researchers identified key genes and compounds to target ferroptosis in triple-negative breast cancer (TNBC). This approach may lead to new therapies for TNBC by targeting the MAPK1 gene and ferroptosis pathways.
Area of Science:
- Oncology
- Bioinformatics
- Computational Biology
Background:
- Triple-negative breast cancer (TNBC) presents a significant therapeutic challenge.
- Ferroptosis, a regulated form of cell death, is implicated in TNBC progression.
- Targeting ferroptosis offers a potential new avenue for TNBC treatment.
Purpose of the Study:
- To identify potential therapeutic compounds targeting ferroptosis in TNBC.
- To uncover key genes and biomarkers associated with ferroptosis in TNBC.
- To evaluate the efficacy of identified compounds against TNBC through computational methods.
Main Methods:
- Bioinformatic analysis of TNBC transcriptomic data from GEO and FerrDb databases.
- Identification of ferroptosis-associated genes and hub genes.
- Computational screening, ADME analysis, molecular docking, and dynamics simulations.
Main Results:
- 140 TNBC-associated ferroptosis genes were identified, with seven hub genes (KRAS, PKM, MAPK1, AR, AURKA, TFRC, ESR1) as potential diagnostic biomarkers.
- Four compounds (DHEA, cinnamaldehyde, glycyrrhetin, shikonin) were found to target MAPK1.
- DHEA, glycyrrhetin, and shikonin showed strong binding affinity to MAPK1, validating them as optimal candidates.
Conclusions:
- Targeting MAPK1-mediated ferroptosis is a promising therapeutic strategy for TNBC.
- The identified compounds (DHEA, glycyrrhetin, shikonin) warrant further investigation for drug development.
- This study provides novel insights into ferroptosis regulation in TNBC.
