ArticleJournal of experimental pharmacology2025
Pyrazoline B Induces Oxidative Stress Mediated Toxicity, Cell Cycle Arrest, and Caspase-Independent Apoptosis in BT-474 Human Breast Cancer Cells.
Article in Journal of experimental pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- 2-Pyrazoline-5-One Derivative Suppresses Cell Proliferation and Induces Apoptosis With Upregulation of Bax in Breast Cancer Cells.Journal of biochemical and molecular toxicology · 2026Article
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Authors and funding
8 authors.
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Abstract
Introduction: Luminal subtype B breast cancer represents a clinically challenging subtype, accounting for nearly 40% of all breast cancers. However, clinical outcomes remain suboptimal due to challenges such as poor solubility, resistance, and drug-induced toxicity. In our previous work, a synthesized compound pyrazoline B demonstrated potent toxicity effects towards T47D, 4T1, and Hs578T breast cancer cells, WiDr colorectal cancer cells, and HeLa cervical cancer cells. Building on these findings, we now investigate-for the first time-the therapeutic potential of a lead compound, pyrazoline B, against luminal B breast cancer using the clinically relevant BT-474 model (HER2+/ER+). This study systematically evaluates pyrazoline B's standalone efficacy and preliminary synergistic interactions with paclitaxel, aiming to address current therapeutic gaps in this high-risk subtype. Methods: Comprehensive in vitro analysis included proliferation and cell migration (scratch) assays, flow cytometry (apoptosis and cell cycle), ELISA (EGFR/VEGFR-2), and RT-qPCR, complemented by in silico ADME and molecular docking analyses. Results: Pyrazoline B demonstrated multimodal activity, inducing G0/G1 arrest through Cyclin D1 suppression while reduced EGFR and VEGFR-2 proteins level. The compound triggered caspase-independent cell death via oxidative stress. Additionally, pyrazoline B enhances the inhibitory effect of paclitaxel on the proliferation and migration of cancer cells. ADME predictions revealed that pyrazoline B exhibits more favorable pharmacokinetic properties of than paclitaxel. Discussion: Our findings established pyrazoline B as a first-in-class multi-target agent against BT-474 luminal B breast cancer, uniquely capable of simultaneously disrupting cell cycle progression, growth factor signaling, and redox homeostasis. Pyrazoline B demonstrates strong potential as a monotherapy, and our initial combination screening showed promising boosting effects when used with existing therapies. Future studies should prioritize: mechanistic synergy studies and in vivo validation to assess translational potential.
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