Table 3.

Novel therapies targeting the ROS-mediated TME alteration.

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]