|
| Therapy | Target | Material type | Mechanism | References |
|
| BEMER electromagnetic field therapy | ROS | Cancer cell lines | Enhanced ROS formation and induced DNA damage | [64] |
| X-ray responsive selenium nanoparticles | ROS | HeLa and NIH3T3 cells | ROS overproduction causing the cell apoptosis | [65] |
| Diisopropylamine dichloroacetate | ROS | Human esophageal squamous cell carcinoma cell lines Eca-109 and TE-13 | Modulated mitochondrial oxidation | [66] |
| Bortezomib, romidepsin | NF-κB | Human NSCLC cell lines (A549) | Increasing ROS and stimulating the extrinsic pathway of apoptosis | [67] |
| Bortezomib | ROS, Noxa | Mantle-cell lymphoma cell lines and patients | Cytotoxic effect through ROS generation and Noxa induction | [68] |
| Celecoxib, 5-FU | ROS | Human squamous cell lines (SNU-1041 and SNU-1076), orthotopic tongue cancer mouse model | Inhibiting the AKT pathway and enhancing ROS production | [69] |
| Selenium nanoparticles | TNF, IRF1 | Human prostate adenocarcinoma cell line (PC-3) | Causing TNF and IRF1-induced ROS-mediated necroptosis | [70] |
| miR-139-5p | Multiple genes | Breast cancer patients, human breast cancer cell line (MCF7), xenograft mouse model | Suppression of gene networks of DNA repair and ROS defense | [71] |
| Ursolic acid | | BGC-823 human adenocarcinoma gastric cancer cell line | Enhanced G2/M arrest, increasing ROS, promoting apoptosis | [72] |
| miR-200c nanoparticles | CSC | Human gastric adenocarcinoma cell lines (BGC823, SGC7901, and MKN45) and an immortalized human gastric mucosa cell line (GES-1) | Impairing ROS generation and DNA repair by the miR-200c | [73] |
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