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Cancer cell membrane-biomimetic and antioxidant-powered nanoplatform for overcoming multidrug resistance in triple-negative breast cancer.

International journal of biological macromolecules 2026 Vol.337(Pt 1) p. 149478

Sun Q, Jin X, Ma Y, Li X, Peng M, Yelebolati S, Cui C

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Triple-negative breast cancer (TNBC) is notoriously refractory to chemotherapy because of multidrug resistance (MDR) driven by P-glycoprotein (P-gp) overexpression and oxidative stress in microenviron

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APA Sun Q, Jin X, et al. (2026). Cancer cell membrane-biomimetic and antioxidant-powered nanoplatform for overcoming multidrug resistance in triple-negative breast cancer.. International journal of biological macromolecules, 337(Pt 1), 149478. https://doi.org/10.1016/j.ijbiomac.2025.149478
MLA Sun Q, et al.. "Cancer cell membrane-biomimetic and antioxidant-powered nanoplatform for overcoming multidrug resistance in triple-negative breast cancer.." International journal of biological macromolecules, vol. 337, no. Pt 1, 2026, pp. 149478.
PMID 41360238

Abstract

Triple-negative breast cancer (TNBC) is notoriously refractory to chemotherapy because of multidrug resistance (MDR) driven by P-glycoprotein (P-gp) overexpression and oxidative stress in microenvironment (TME). To overcome this, we engineered a triple-action biomimetic nanoplatform (BSA-OPC/siMDR1@CCM) co-encapsulating oligomeric proanthocyanidins (OPC) and MDR1-targeting siRNA (siMDR1) within cancer cell membrane (CCM) cloaked bovine serum albumin (BSA) nanoparticles. The precision-engineered nanoplatform achieved >89 % OPC encapsulation efficiency, complete siMDR1 complexation, pH-responsive drug release (26 % at tumor-mimetic pH 6.5 vs <5 % at systemic pH 7.4), and robust nuclease resistance. In vitro, enhanced cellular uptake and enabled lysosomal escape, achieving 65 % MDR1 knockdown and 85 % ROS suppression to synergistically restore doxorubicin (DOX) sensitivity. In vivo, the nanoplatform showed 7.7-fold greater tumor accumulation versus controls, driving 68 % tumor regression and 100 % 30-day survival in MDR-4T1 models while abolishing metastases. Mechanistic studies confirmed downregulation of P-gp, p53, Ki67, HIF-1α, and ROS without systemic toxicity. This integrated strategy combining targeted delivery, genetic resistance reversal, and microenvironment remodeling, represents a potential strategy against chemorefractory TNBC.

MeSH Terms

Triple Negative Breast Neoplasms; Humans; Drug Resistance, Neoplasm; Drug Resistance, Multiple; Animals; Female; Cell Line, Tumor; Doxorubicin; Antioxidants; Nanoparticles; Mice; Cell Membrane; RNA, Small Interfering; Biomimetic Materials; ATP Binding Cassette Transporter, Subfamily B

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