Table 7.

Literature queries on drugs interacting with key genes.

Drug	Remark	Mechanism of ferroptosis	Reference
Decitabine	Yu et al. indicated that decitabine increased the sensitivity of TNBC cells to DNA methyltransferase (DNMT) by inducing ubiquitination and degradation of the E3 ligase TNF receptor-associated factor 6 (TRAF6).		(41)
	Nakajima et al. illustrated that decitabine induced the expression of the B-cell lymphoma-2 (Bcl2) family protein NOXA.	antioxidant defence	(42)
	Ohshima-Hosoyama et al. indicated that NOXA could promote oxidative stress-induced cell death in medulloblastoma cell lines.		(43)
	Brglez et al. found that decitabine induced mRNA expression of phospholipase A2-related proteins Phospholipase A2 group IIA (PLA2G2A), Phospholipase A2 group III (PLA2G3) and Phospholipase A2 group X (PLA2G10) in TNBC, which in turn led to cell apoptosis.	lipid peroxidation	(44)
Rosiglitazone	Mody et al. indicated that rosiglitazone inhibited the viability and DNA synthesis of breast cancer cells, which in turn enhanced the sensitivity of tumor cells to tumor necrosis factor alpha (TNFα) and ultimately induced cell apoptosis.		(45)
	Ishay-Ronen et al. showed that rosiglitazone in combination with the MEK inhibitor trametinib enhanced epithelial differentiation and adipogenesis in vivo and in vitro, thus promoting the conversion of invasive breast cancer cells into adipocytes, and ultimately inhibiting the metastasis of cancer cells.	lipid peroxidation	(46)
1-Methyl-3-isobutylxanthine	1-Methyl-3-isobutylxanthine is also known as 3-isobutyl-1-methylxanthine (IBMX). Lv et al. indicated that IBMX decreased the proliferation and invasion of glioma stem cells by activating the cAMP signaling pathway and inhibiting the mitogen-activated protein kinases (MAPK) signaling pathway.		(47)
	Crumpton et al. found that IBMX induced the production of reactive oxygen in breast cancer cells and enhanced the sensitivity of cells to other oxidants, which in turn led to apoptosis.	antioxidant defence	(48)
	Lee et al. indicated that IBMX promoted tyrosinase activity and activated melanin production.	antioxidant defence	(49)
	Hill et al. indicated that melanin could generate destructive reactive oxygen and enhance DNA damage, leading to cell death.		(50)

represents that the drug could inhibit the progression of TNBC by experiment.

represents that the drug could inhibit the progression of the breast tumor by experiment.

represents that the drug could inhibit the progression of other tumor by experiment.