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Updated: Aug 16, 2026
Ex Vivo Treatment Response of Primary Tumors and/or Associated Metastases for Preclinical and Clinical Development of Therapeutics
Published on: October 2, 2014
Plasma-activated solutions potentiate the antitumor effects of HIPEC via endoplasmic reticulum stress mediated
Tuanhe Sun1, Yuyi Ma2, Yuanchang Peng2
1Department of Surgical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China; State Key Laboratory of Electrical Insulation and Power Equipment, School of Electrical Engineering, Xi'an Jiaotong University, Xi'an, Shaanxi, 710049, China.
Hyperthermic intraperitoneal chemotherapy (HIPEC) is a promising therapy for peritoneal metastasis, yet variable efficacy and complications necessitate improvement. This study investigates plasma-activated solutions (PAS) as an enhancer of HIPEC against colorectal cancer-derived peritoneal metastasis. Using murine models and human colorectal cancer cell lines, PAS combined with HIPEC significantly suppresses tumor growth, reduces malignant ascites, and improves survival. Mechanistically, PAS induces oxidative stress, activating the endoplasmic reticulum stress (ER-stress) pathway to trigger cancer cell death. Reactive oxygen species (ROS) are critical mediators, as their neutralization abolishes antitumor effects. Furthermore, integrating PAS-HIPEC with anti-PD-L1 immunotherapy yields synergistic tumor control and survival benefits superior to monotherapies. These findings establish PAS-enhanced HIPEC as a promising strategy that leverages ROS-mediated cell death to potentiate chemotherapy and sensitize tumors to immunotherapy, offering a novel approach for this challenging disease.
Hyperthermic intraperitoneal chemotherapy (HIPEC) is a promising therapy for peritoneal metastasis, yet variable efficacy and complications necessitate improvement. This study investigates plasma-activated solutions (PAS) as an enhancer of HIPEC against colorectal cancer-derived peritoneal metastasis. Using murine models and human colorectal cancer cell lines, PAS combined with HIPEC significantly suppresses tumor growth, reduces malignant ascites, and improves survival. Mechanistically, PAS induces oxidative stress, activating the endoplasmic reticulum stress (ER-stress) pathway to trigger cancer cell death. Reactive oxygen species (ROS) are critical mediators, as their neutralization abolishes antitumor effects. Furthermore, integrating PAS-HIPEC with anti-PD-L1 immunotherapy yields synergistic tumor control and survival benefits superior to monotherapies. These findings establish PAS-enhanced HIPEC as a promising strategy that leverages ROS-mediated cell death to potentiate chemotherapy and sensitize tumors to immunotherapy, offering a novel approach for this challenging disease.
