Table 2.

Cuproptosis and CRGs in cancers

Cancer types	Important CRGs	Advances of cuproptosis in cancer	References
HCC	LIPT1, LIAS, PDHB, DLD, CDKN2A, GLS, DLAT	MELK → PI3K/mTOR pathway→ DLAT↑ → tumor progression	[100, 101, 106, 109, 111, 115, 122, 132–134]
HNSCC	FDX1, DLAT, PDHB, AURKA	OLR1↓ → DLAT oligomerization↑ → cuproptosis AURKA↓ → tumor suppression	[90, 95, 111, 137, 138]
GC	MTF1, SERPINE1, FDX1	Cu↑ → METTL16 lactylation→ FDX1↑ → cuproptosis	[130, 140, 141]
CRC	CDKN2A, DLAT, DLD, PDHB, FDX1	4-OI → targeting GAPDH → aerobic glycolysis↓→ cuproptosis FDX1↓ → impair 4-OI → cuproptosis↓	[142–145]
ccRCC	FDX1, PDHA1, LIAS, PDHB, DLD, CDKN2A	MiR-21-5p → FDX1↓ →tumor progression ADM↑ → p38/MAPK pathway→ FOXO3↑→ cuproptosis↓ and sunitinib resistant	[90, 92, 95, 106, 107, 109, 112, 113, 123, 146, 147]
NSCLC	LIPT1	DSF→ ATP7B↑ →HIF-1 pathway → PD-L1↑ →tumor immune escape LIPT1↑ → ATOX1↓ → tumor suppression CuET→ bypass GSH→ cuproptosis	[54, 99, 148–150]
BLCA	DLD, PDE3B	PDE3B→KRT6B keratinization and sensitivity of tumor to copper ionophores↑ → tumor suppression GOx@[Cu(tz)] → glucose↓ → cuproptosis sensitivity↑	[115, 151–153]
OS	FDX1, LIPT1, DLAT	T-HCN@CuMS → cuproptosis and cuproptosis sensitivity↑ TFP-Cu → Immune response↑ and cuproptosis→ tumor suppression MCD → ROS↑ → cuproptosis	[91, 157–159]
CCA	FDX1, PDHA1, LIAS, DLD,	CD274↓ → FDX1↓ →cuproptosis sensitivity↑	[90, 106, 109, 115, 160, 161]
OC	MTF1, WASF2	CTC-246B18.8↑ → poor prognosis Anisomycin→ YY1↓ → cuproptosis	[129, 164, 166, 167]
Glioma and GBM	FDX1, PDHA1, DLD, GLS, CDKN2A, SLC31A1	miR-606 → targeting FDX1→ tumor suppression LEF1-AS1↓ → tumor suppression HFn-Cu-REGO NPs → autophagy blockade and cuproptosis → tumor suppression	[90, 106, 115, 123, 126, 168–171, 174]
PDAC	GLS	HBO → efficacy of CuET@PH NPs↑ → tumor suppression	[126, 177, 178]
AML	LIPT1, MTF1, GLS, CDKN2A FDX1, LIAS, DLD, DLAT, PDHA1, SLC31A1, ATP7B	UM4118 → cuproptosis	[89, 90, 115, 123, 181]