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Isobavachalcone Induces Multiple Cell Death in Human Triple-Negative Breast Cancer MDA-MB-231 Cells
Cheng-Zhu Wu1,2, Mei-Jia Gao1, Jie Chen1
1School of Pharmacy, Bengbu Medical College, 2600 Donghai Road, Bengbu 233030, China.
Abstract:
Standardized treatment guidelines and effective drugs are not available for human triple-negative breast cancer (TNBC). Many efforts have recently been exerted to investigate the efficacy of natural compounds as anticancer agents owing to their low toxicity. However, no study has examined the effects of isobavachalcone (IBC) on the programmed cell death (PCD) of human triple-negative breast MDA-MB-231 cancer cells. In this study, IBC substantially inhibited the proliferation of MDA-MB-231 cells in concentration- and time-dependent manners. In addition, we found that IBC induced multiple cell death processes, such as apoptosis, necroptosis, and autophagy in MDA-MB-231 cells. The initial mechanism of IBC-mediated cell death in MDA-MB-231 cells involves the downregulation of Akt and p-Akt-473, an increase in the Bax/Bcl-2 ratio, and cleaved caspases-3 induced apoptosis; the upregulation of RIP3, p-RIP3 and MLKL induced necroptosis; as well as a simultaneous increase in LC3-II/I ratio induced autophagy. In addition, we observed that IBC induced mitochondrial dysfunction, thereby decreasing cellular ATP levels and increasing reactive oxygen species accumulation to induce PCD. These results suggest that IBC is a promising lead compound with anti-TNBC activity.
Insights
Isoflavonoid isobavachalcone (IBC) effectively inhibits triple-negative breast cancer (TNBC) cell growth. IBC triggers multiple programmed cell death pathways, including apoptosis, necroptosis, and autophagy, offering a potential new treatment for TNBC.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Triple-negative breast cancer (TNBC) lacks standardized treatments and effective drugs.
- Natural compounds are explored for anticancer potential due to low toxicity.
- The effect of isobavachalcone (IBC) on programmed cell death in TNBC cells was unexamined.
Purpose of the Study:
- To investigate the anti-cancer effects of isobavachalcone (IBC) on human triple-negative breast cancer MDA-MB-231 cells.
- To elucidate the mechanisms of IBC-induced programmed cell death (PCD) in these cancer cells.
Main Methods:
- Cell proliferation assays to assess IBC's impact on MDA-MB-231 cell growth.
- Analysis of apoptosis, necroptosis, and autophagy markers following IBC treatment.
- Assessment of mitochondrial function, including ATP levels and reactive oxygen species (ROS) production.
Main Results:
- IBC significantly inhibited MDA-MB-231 cell proliferation in a dose- and time-dependent manner.
- IBC induced apoptosis (via Akt/Bax/Bcl-2/caspase-3 pathways), necroptosis (via RIP3/MLKL pathways), and autophagy (via LC3-II/I ratio).
- IBC caused mitochondrial dysfunction, reduced ATP levels, and increased ROS accumulation, contributing to PCD.
Conclusions:
- Isoflavonoid isobavachalcone (IBC) demonstrates significant anti-proliferative effects against human triple-negative breast cancer cells.
- IBC induces multiple programmed cell death pathways, including apoptosis, necroptosis, and autophagy.
- IBC shows promise as a lead compound for developing novel anti-TNBC therapies.
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