Table 2.

Overview of nanoparticles induce ferroptosis to activate cGAS-STING in cancer treatment

Nanoparticles	Loaded agent	Cancer	Tested model	Effects OR Involved mechanism	Ref
Cu/ZIF-8@U-104@siNFS1-HA		Osteosarcoma	MG-63 tumor-bearing C57BL/6J mice	ZCUNH synergize ferroptosis induction to boost immunotherapy by activating cGAS-STING pathway in osteosarcoma.	[37]
DHA@MIL-101	U-104	NSCLC	Lewis lung cancer cells tumor-bearing C57 mice	DHA@MIL-101 enhances anti-cancer immunotherapy by inducing Ferroptosis to activate cGAS-STING for reprogramming of macrophage.	[38]
Exo@MnIO&BG	Dihydroartemisinin	Breast cancer	4T1 tumor-bearing mice	Exo@MnIO&BG enhances anti-cancer immunotherapy by boosting ferroptosis to activate cGAS-STING.	[140]
Fe-THBQ/SR	SR-717	Breast cancer	4T1 tumor-bearing mouse	Fe-THBQ/SR promotes tumor immunotherapy via synergistic ferroptosis and STING activation.	[141]
CMS	Ca²⁺ & Mn	TNBC	4T1-tumor-bearing mice	The CMS-induced ferroptosis- and Mn²⁺-mediated STING pathway activation promoted tumor -associated macrophage (TAM) polarization toward antitumor phenotypes and dendritic cell (DC) maturation for antigen presentation.	[142]
MG-LAAO	Gallium -magnesium	Breast cancer	4T1-tumor-bearing mice	MG-LAAO blocks tumor cell autophagy, neutralizes acidic TME via H⁺ scavenging, and inhibits lactic acid accumulation, thereby dismantling cytoprotective mechanisms and preventing immune evasion.	[143]
MMP NDs	Mo/Mn	CRC	CT26 tumor bearing mice.	MMP NDs exploit the synergistic redox activity of high-valence Mo/Mn to deplete tumor-overexpressed glutathione (GSH), inducing ferroptosis while activating the cGAS-STING pathway to amplify antitumor immunity. This dual mechanism triggers a self-reinforcing therapeutic cycle: ferroptosis releases tumor antigens, activating CD8⁺ T cells to secrete interferon-γ (IFN-γ), which suppresses GPX4 expression and exacerbates lipid peroxidation, thereby sustaining ferroptotic cell death.	[144]
BQR@MLipo	Brequinar	Breast cancer	4T1-tumor-bearing mice	BQR@MLipo inhibit DHODH to trigger mitochondrial LPO and ROS overproduction, resulting in ferroptosis. This process releases immunogenic damage-associated molecular patterns (DAMPs), including calreticulin (CRT), ATP, and HMGB1, while mitochondrial DNA (mtDNA) leakage activates the cGAS-STING pathway to stimulate IFN-β secretion.	[145]
HBMn-FA	Hemin, BSO and Mn2+	Breast cancer	4T1-tumor-bearing mice	HBMn-FA nanoplatform drives ferroptosis in tumor cells, generating high levels of ROS that induce mitochondrial stress and release endogenous mtDNA, which synergizes with Mn²⁺ to activate the cGAS-STING pathway, while tumor-derived cytosolic dsDNA from ferroptotic cell debris further amplifies STING signaling in dendritic cells (DCs) and other antigen-presenting cells.	[146]
HMG nanoparticles		Breast cancer	4T1-tumor-bearing mice	HMG induces ferroptosis to intensify DNA damage in 4T1 breast cancer cells and synergizes with radiotherapy to activate the Mn²⁺-mediated cGAS-STING pathway, triggering robust systemic antitumor immunity.	[147]

DHODH, dihydroorotate dehydrogenase; U-104,a novel carbonic anhydrase inhibitor