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Translational selenium nanoparticles trigger apoptosis in triple-negative breast cancer cells through the MAPKs/Bcl2
Binhua Zou1, Shuoshan Li2, Kar-Him Luk3
1Department of Rehabilitation Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, PR China.
Abstract:
Triple-negative breast cancer (TNBC) is characterized by aggressive biological behavior, including rapid post-treatment recurrence propensity, heightened metastatic dissemination, and significantly diminished survival outcomes. These features emphasize the necessity for innovative therapeutic strategies in TNBC treatment. Herein, we developed selenium nanoparticles modified with a mushroom polysaccharide-protein complex (PTR-SeNPs) and evaluated them in vitro anti-tumor efficacy across 17 human TNBC cell lines, followed by elucidation of the mechanism underlying PTR-SeNPs-induced apoptosis. In vitro evaluation across TNBC cell models revealed that PTR-SeNPs exhibit promising anti-tumor efficacy with preferential induction of mitochondrial-dependent apoptosis, demonstrating significant cytotoxic efficacy through MAPKs/Bcl2 pathway. Notably, further conjugation of PTR-SeNPs with anti-human MUC1 antibodies generated dual-modified nanoparticles (MUC1@PTR-SeNPs), which significantly enhanced anti-tumor activity in five TNBC cell lines with high/medium MUC1 expression. Furthermore, oral administration of MUC1@PTR-SeNPs for 30 days markedly inhibited tumor growth in mice bearing MDA-MB-468 xenografts via induction of mitochondria-mediated apoptosis. This work highlights the therapeutic potential of PTR-SeNPs against human TNBC, elucidates their molecular mechanisms, metabolic profile, and toxicity, thereby advancing this novel nano-mineral as a future treatment strategy for TNBC.
Insights
New selenium nanoparticles (PTR-SeNPs) show potent anti-tumor effects against triple-negative breast cancer (TNBC) by inducing apoptosis. Dual-modified nanoparticles (MUC1@PTR-SeNPs) further enhanced efficacy, offering a promising nano-mineral treatment strategy for TNBC.
Area of Science:
- Biomedical Engineering
- Nanotechnology
- Oncology
Background:
- Triple-negative breast cancer (TNBC) presents aggressive behavior, rapid recurrence, and poor survival rates, necessitating novel therapeutic approaches.
- Current treatments for TNBC are limited, highlighting the need for innovative strategies to improve patient outcomes.
Purpose of the Study:
- To develop and evaluate selenium nanoparticles (PTR-SeNPs) modified with a mushroom polysaccharide-protein complex for their anti-tumor efficacy against TNBC.
- To elucidate the mechanism of action of PTR-SeNPs, focusing on apoptosis induction.
- To enhance the anti-tumor activity of PTR-SeNPs by conjugating them with anti-MUC1 antibodies (MUC1@PTR-SeNPs) for targeted delivery.
Main Methods:
- *In vitro* anti-tumor efficacy of PTR-SeNPs was assessed across 17 human TNBC cell lines.
- Mechanism of PTR-SeNPs-induced apoptosis was investigated, including the involvement of the MAPKs/Bcl2 pathway and mitochondrial-dependent apoptosis.
- MUC1@PTR-SeNPs were synthesized and evaluated for enhanced anti-tumor activity in TNBC cell lines with varying MUC1 expression levels.
- *In vivo* anti-tumor effects of MUC1@PTR-SeNPs were evaluated in a mouse xenograft model (MDA-MB-468).
Main Results:
- PTR-SeNPs demonstrated significant *in vitro* anti-tumor efficacy against TNBC cell lines, primarily through inducing mitochondrial-dependent apoptosis via the MAPKs/Bcl2 pathway.
- MUC1@PTR-SeNPs exhibited enhanced anti-tumor activity compared to PTR-SeNPs in TNBC cell lines with high/medium MUC1 expression.
- Oral administration of MUC1@PTR-SeNPs significantly inhibited tumor growth in a TNBC xenograft mouse model by inducing mitochondria-mediated apoptosis.
Conclusions:
- PTR-SeNPs possess promising therapeutic potential against human TNBC.
- MUC1@PTR-SeNPs offer an enhanced, targeted therapeutic strategy for TNBC.
- This study advances novel nano-minerals as a potential future treatment for TNBC, with elucidated mechanisms and safety profiles.
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