Interplay between Mitochondrial Metabolism and Cellular Redox State Dictates Cancer Cell Survival

Table 1

Summary of the various mitochondrial-related therapeutics in targeting tumor progression.

Category	Drug name	Mechanism	References
Complex I inhibitors	Metformin	Inhibits complex I, disrupting ATP production by OXPHOS.	[170]
	IACS-010759		[171–173]
	OPB-51602		[174, 175]
ATP synthase inhibitors	Oligomycin	Induces heightened superoxide production and apoptosis in tumors.	[178, 179]
	Gboxin	Restricts ATP synthase, increases mitochondria membrane potential.	[180]
Mitochondria biogenesis targeting compounds	Gamitinib	Specifically inhibits tumor mitochondrial HSP90 and induces mitochondria apoptosis.	[182–185]
	Doxycycline	Inhibits mitochondrial biogenesis in bacterial and mammalian cells and reduces mitochondrial translation.	[187, 188]
Inhibitors of mitochondria dynamics	Mitochondrial division inhibitor (e.g., Mdivi 1)	Inhibits mitochondrial fission which prevents cell cycle progression and hence suppresses tumor growth.	[191–194]
SOD mimetics	Manganese porphyrins (e.g., MnTnHex 2 PyP5+)	Mimics MnSOD activity; increases cellular ROS levels, and ultimately induces cell death. Also inhibits cell migration and invasion.	[198, 199]
	Nitroxides (e.g., Mito TEMPOL)	Antioxidative function; induces DNA damage, apoptosis, and mitochondrial distress in tumors.	[200, 201]
Bcl-2 inhibitors	ABT-263 (Navitoclax)	BH3 mimetic that targets antiapoptotic Bcl-2 and Bcl-xL.	[206, 207]
	ABT-737
	ABT-199 (Venetoclax)	BH3 mimetic that has affinity for antiapoptotic Bcl-2.	[209–213]