Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0076)
Name
Sulfasalazine
Synonyms
sulfasalazine; 599-79-1; Salicylazosulfapyridine; Azulfidine; Salazosulfapyridine; Sulphasalazine; Salazopyrin; Asulfidine; Benzosulfa; Salazopyridin; Accucol; Azopyrin; Sulcolon; Colo-Pleon; Salazopiridazin; Azopyrine; Reupirin; Salisulf; Salazosulfapyridin; Sulfasalazinum; w-t Sasp oral; Azulfidine EN; Sulfasalazin; Sulfasalazina; Sulfazalazine; Azulfidine EN-tabs; Salazosulfapiridina; Salazosulfapyridinum; Sas-500; SASP; 5-(p-(2-Pyridylsulfamyl)phenylazo)salicylic acid; NSC 667219; S.A.S.-500; 5-(4-(2-Pyridylsulfamoyl)phenylazo)-2-hydroxybenzoic acid; 4-(Pyridyl-2-amidosulfonyl)-3'-carboxy-4'-hydroxyazobenzene; 5-((p-(2-Pyridylsulfamoyl)phenyl)azo)salicylic acid; 2-Hydroxy-5-((4-((2-pyridinylamino)sulfonyl)phenyl)azo)benzoic acid; 5-[4-(2-Pyridylsulfamoyl)phenylazo]salicylic Acid; CHEBI:9334; NSC 203730; S.A.S. 500; C18H14N4O5S; (E)-2-hydroxy-5-((4-(N-(pyridin-2-yl)sulfamoyl)phenyl)diazenyl)benzoic acid; Sulfasalazopyridine; MFCD00057363; Benzoic acid, 2-Hydroxy-5-[[4-[(2-pyridinylamino)sulfonyl]phenyl]azo]-; 3XC8GUZ6CB; Sulfasalazine (Azulfidine); NSC-203730; NSC-667219; Benzoic acid, 2-hydroxy-5-((4-((2-pyridinylamino)sulfonyl)phenyl)azo)-; S.A.S.; 737754-28-8; Azosulfidin; DTXSID0021256; 2-hydroxy-5-{[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl}benzoic acid; 5-[p-(2-Pyridylsulfamoyl)phenylazo]salicylic acid; 2-HYDROXY-(5-([4-(2-PYRIDINYLAMINO)SULFONYL]PHENYL)AZO)BENZOIC ACID; 5-(p-(2-Pyridinylsulfamoyl)Phenylazo)Salicylic Acid; NSC203730; NSC667219; Salicylic acid, 5-((p-(2-pyridylsulfamoyl)phenyl)azo)-; SSZ; NCGC00090903-01; Salazo-sulfapyridinum; CAS-599-79-1; 2-hydroxy-5-[[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl]benzoic acid; 2-Hydroxy-5-[[4-[(2-pyridinylamino)sulfonyl]phenyl]azo]benzoic acid; 2-hydroxy-5-[(E)-{4-[(pyridin-2-ylamino)sulfonyl]phenyl}diazenyl]benzoic acid; 5-[p-(2-Pyridylsulfamyl)phenylazo]salicylic acid; (3Z)-6-Oxo-3-[[4-(pyridin-2-ylsulfamoyl)phenyl]hydrazinylidene]cyclohexa-1,4-diene-1-carboxylic acid; 5-(p-(2-Pyridylsulfamoyl)phenylazo)salicylic acid; Salazopyrin EN-Tabs; DTXCID401256; Sulfasalazinum [INN-Latin]; Sulfasalazina [INN-Spanish]; Salicylic acid, 5-[[p-(2-pyridylsulfamoyl)phenyl]azo]-; 2-Hydroxy-5-[4-(pyridin-2-ylsulfamoyl)-phenylazo]-benzoic acid; Salazosulfapyridinum [INN-Latin]; Salazosulfapiridina [INN-Spanish]; SI-88; 2-Hydroxy-5-((4-(N-(pyridin-2-yl)sulfamoyl)phenyl)diazenyl)benzoic acid; Alti-Sulfasalazine; PMS-Sulfasalazine; 2-hydroxy-5-[(E)-2-{4-[(pyridin-2-yl)sulfamoyl]phenyl}diazen-1-yl]benzoic acid; Azulfidine (TN); SMR000059146; Azlufidine EN-Tabs; Sulphasalazine, N-; CCRIS 4713; HSDB 3395; 13gs; Pms-Sulfasalazine E.C.; SR-05000001721; EINECS 209-974-3; UNII-3XC8GUZ6CB; 5-[[p-(2-Pyridylsulfamoyl)phenyl]azo]salicylic acid; Sulfasalazine (USP/INN); S.A.S. Enteric-500; BRN 0356241; Iwata; Prestwick_848; Sulfasalazine [USAN:USP:INN:BAN]; Spectrum_000998; Prestwick0_000520; Prestwick1_000520; Prestwick2_000520; Prestwick3_000520; Spectrum2_001216; Spectrum3_001364; Spectrum4_000347; Spectrum5_001443; SULFASALAZINE [MI]; CHEMBL421; Epitope ID:122672; SULFASALAZINE [INN]; SCHEMBL4514; SCHEMBL4515; Salazosulfapyridine (JP17); SULFASALAZINE [HSDB]; SULFASALAZINE [IARC]; SULFASALAZINE [USAN]; SCHEMBL18490; BSPBio_000479; BSPBio_002888; KBioGR_000753; KBioGR_002314; KBioSS_001478; KBioSS_002316; SULFASALAZINE [VANDF]; 5-22-08-00433 (Beilstein Handbook Reference); MLS000759399; MLS001424109; MLS006011702; BIDD:GT0161; DivK1c_000860; SPECTRUM1500552; SULFASALAZINE [MART.]; SPBio_001032; SPBio_002400; SULFASALAZINE [USP-RS]; SULFASALAZINE [WHO-DD]; SULFASALAZINE [WHO-IP]; 5-[4-(2-Pyridylsulfamoyl)-phenylazo]-salicylic acid; BPBio1_000527; CHEMBL100848; CHEMBL242373; GTPL4840; SCHEMBL1079598; SCHEMBL1229516; CHEMBL1206016; SCHEMBL10289061; CHEBI:94500; HMS502K22; KBio1_000860; KBio2_001478; KBio2_002314; KBio2_004046; KBio2_004882; KBio2_006614; KBio2_007450; KBio3_002108; KBio3_002794; SALAZOSULFAPYRIDINE [JAN]; cMAP_000018; NCEXYHBECQHGNR-QZQOTICOSA-N; NCEXYHBECQHGNR-UHFFFAOYSA-N; NINDS_000860; OQANPHBRHBJGNZ-BKUYFWCQSA-N; OQANPHBRHBJGNZ-UHFFFAOYSA-N; HMS1569H21; HMS1921C05; HMS2051J21; HMS2090P13; HMS2092K07; HMS2096H21; HMS2232H07; HMS3370D16; HMS3393J21; HMS3655G07; HMS3713H21; HMS3871J13; HMS3884E21; Pharmakon1600-01500552; SULFASALAZINE [ORANGE BOOK]; BCP13311; SULFASALAZINE [EP MONOGRAPH]; Tox21_111037; Tox21_201239; Tox21_300541; BDBM50097125; BDBM50103596; CCG-39145; DL-510; NSC757330; s1576; SULFASALAZINE [USP MONOGRAPH]; SULFASALAZINUM [WHO-IP LATIN]; 2-hydroxy-5-(2-{4-[(pyridin-2-yl)sulfamoyl]phenyl}diazen-1-yl)benzoic acid; AKOS002311709; AKOS025116975; AKOS026749974; AKOS037515748; Tox21_111037_1; WLN: T6NJ BSWMR DNUNR DQ CVQ; CCG-100987; DB00795; HS-0062; NC00237; NSC-757330; IDI1_000860; SMP2_000059; NCGC00016518-01; NCGC00090903-02; NCGC00090903-03; NCGC00090903-04; NCGC00090903-05; NCGC00090903-06; NCGC00090903-07; NCGC00090903-08; NCGC00090903-09; NCGC00090903-11; NCGC00186644-01; NCGC00254313-01; NCGC00258791-01; AC-20497; HY-14655; PD087097; SMR004703430; SY052318; SBI-0051526.P003; FT-0603483; FT-0674746; S0580; SW196979-4; C07316; D00448; EN300-119546; H10652; AB00052101-04; AB00052101-06; AB00052101_07; AB00052101_08; A832559; Q420035; Q-201769; SR-05000001721-1; SR-05000001721-2; SR-05000001721-3; Sulfasalazine, analytical standard, >=98% (HPLC); 5-[[4-(2-Pyridylsulfamoyl)phenyl]azo]salicylic acid; BRD-K10670311-001-06-4; BRD-K10670311-001-08-0; Q27166356; Q63398427; Sulphasalazine, Antibiotic for Culture Media Use Only; F2173-1125; Z1521554012; 4-(Pyridyl-2-amidosulfonyl)-3''-carboxy-4''-hydroxyazobenzene; Sulfasalazine, European Pharmacopoeia (EP) Reference Standard; 2-hydroxy-5-[(E)-[4-(2-pyridylsulfamoyl)phenyl]azo]benzoic acid; 5-{4-[(2-pyridylideneamino)sulfonyl]phenyldiazenyl}salicylic acid; Sulfasalazine, United States Pharmacopeia (USP) Reference Standard; (E)-2-hydroxy-5-((4-(N-pyridin-2-ylsulfamoyl)phenyl)diazenyl)benzoic acid; 2-hydroxy-5-((4-(N-pyridin-2-ylsulfamoyl)phenyl)diazenyl)benzoic acid; 2-Hydroxy-5-((4-[(2-pyridinylamino)sulfonyl]phenyl)diazenyl)benzoic acid #; 2-hydroxy-5-{(E)-[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl}benzoic acid; 2-HYDROXY-5-((4-((2-PYRIDINYLAMINO)SULFONYL)PHENYL)AZO)BENZOIC ACID [WHO-IP]; 6-oxo-3-(2-[4-(n-pyridin-2-ylsulfamoyl)phenyl]hydrazono)cyclohexa-1,4-dienecarboxylic acid; BENZOIC ACID, 2-HYDROXY-5-(2-(4-((2-PYRIDINYLAMINO)SULFONYL)PHENYL)DIAZENYL)-; 6-oxo-3-((4-(pyridin-2-ylsulfamoyl)phenyl) hydrazinylidene]cyclohexa-1,4-diene-1-carboxylic acid; 6-oxo-3-[[4-(2-pyridinylsulfamoyl)phenyl]hydrazinylidene]-1-cyclohexa-1,4-dienecarboxylic acid

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Structure
Formula
C18H14N4O5S
IUPAC Name
2-hydroxy-5-[[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl]benzoic acid
Canonical SMILES
C1=CC=NC(=C1)NS(=O)(=O)C2=CC=C(C=C2)N=NC3=CC(=C(C=C3)O)C(=O)O
InChI
InChI=1S/C18H14N4O5S/c23-16-9-6-13(11-15(16)18(24)25)21-20-12-4-7-14(8-5-12)28(26,27)22-17-3-1-2-10-19-17/h1-11,23H,(H,19,22)(H,24,25)
InChIKey
NCEXYHBECQHGNR-UHFFFAOYSA-N
PubChem CID
5339
Full List of Ferroptosis Target Related to This Drug
Cystine/glutamate transporter (SLC7A11)
 Target Info 
In total 5 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Suppressor
Responsed Disease Colon cancer ICD-11: 2B90
 Disease Info 
Responsed Regulator 5'-AMP-activated protein kinase catalytic subunit alpha-2 (PRKAA2) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
AMPK signaling pathway hsa04152
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
PANC-1 cells Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Calu-1 cells Lung squamous cell carcinoma Homo sapiens CVCL_0608
HeLa cells Endocervical adenocarcinoma Homo sapiens CVCL_0030
HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
To generate murine subcutaneous tumors, 5 x 106 HCT116, CX-1, or HT1080 cells in 100 ul phosphate buffered saline (PBS; Thermo Fisher Scientific, AM9625) were injected subcutaneously right of the dorsal midline in athymic nude immunodeficient mice (six- to eight-week-old, female). To generate orthotopic tumors, 1 x 106 KPC cells in 10 ul PBS were surgically implanted into the pancreases of immunocompetent C57BL/6J mice (six- to eight-week-old, female).

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Response regulation BECN1 plays a novel role in lipid peroxidation that could be exploited to improve anticancer therapy by the induction of ferroptosis. Mechanistically, phosphorylation of BECN1 at Ser90/93/96 by PRKAA/ AMPK contributes to the formation of a BECN1-SLC7A11 complex and system Xc-inhibition. Knockdown of BECN1 by shRNA inhibits ferroptosis induced by system X-c- inhibitors (e.g., erastin, sulfasalazine, and sorafenib) in Colon carcinoma.
Experiment 2 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Suppressor
Responsed Disease Colon cancer ICD-11: 2B90
 Disease Info 
Responsed Regulator 5'-AMP-activated protein kinase catalytic subunit alpha-2 (PRKAA2) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
AMPK signaling pathway hsa04152
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
PANC-1 cells Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Calu-1 cells Lung squamous cell carcinoma Homo sapiens CVCL_0608
HeLa cells Endocervical adenocarcinoma Homo sapiens CVCL_0030
HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
To generate murine subcutaneous tumors, 5 x 106 HCT116, CX-1, or HT1080 cells in 100 ul phosphate buffered saline (PBS; Thermo Fisher Scientific, AM9625) were injected subcutaneously right of the dorsal midline in athymic nude immunodeficient mice (six- to eight-week-old, female). To generate orthotopic tumors, 1 x 106 KPC cells in 10 ul PBS were surgically implanted into the pancreases of immunocompetent C57BL/6J mice (six- to eight-week-old, female).

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Response regulation BECN1 plays a novel role in lipid peroxidation that could be exploited to improve anticancer therapy by the induction of ferroptosis. Mechanistically, phosphorylation of BECN1 at Ser90/93/96 by PRKAA/AMPK contributes to the formation of a BECN1-SLC7A11 complex and system Xc-inhibition. Knockdown of BECN1 by shRNA inhibits ferroptosis induced by system X-c- inhibitors (e.g., erastin, sulfasalazine, and sorafenib) in Colon carcinoma.
Experiment 3 Reporting the Ferroptosis-centered Drug Act on This Target [3]
Target for Ferroptosis Suppressor
Responsed Disease Breast cancer ICD-11: 2C60
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
Response regulation The combined effects of vorinostat with salazosulfapyridine (SASP) depend on the accumulation of ROS caused by a decrease in intracellular GSH levels, possibly due to SASP-mediated inhibition of xCT. xCT (coded by the SLC7A11 gene), a light chain subunit of the glutamate-cystine antiporter system Xc(-) in Breast adenocarcinoma.
Experiment 4 Reporting the Ferroptosis-centered Drug Act on This Target [4]
Target for Ferroptosis Suppressor
Responsed Disease Breast cancer ICD-11: 2C60
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model MCF-7 cells Breast carcinoma Homo sapiens CVCL_0031
T-47D cells Invasive breast carcinoma Homo sapiens CVCL_0553
HCC1937 cells Breast ductal carcinoma Homo sapiens CVCL_0290
Bcap37 cells Breast carcinoma Homo sapiens CVCL_0164
HBL-100 cells Normal Homo sapiens CVCL_4362
MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
BT-549 cells Invasive breast carcinoma Homo sapiens CVCL_1092
In Vivo Model
T47D xenografts were established in 5-week-old nude mice (Shanghai SLAC Laboratory Animal Corporation) by inoculating 1 x 107 cells mixed with Matrigel (BD Biosciences) at 1:1 ratio (volume) into the abdominal mammary fat pad. When the tumor reached 50-100 mm3, the mice were assigned randomly into different treatment groups (DMSO, Metformin, SAS, and Metformin + SAS groups). Metformin (200 mg/kg/day) was provided in drinking water. Sulfasalazine was dissolved in dimethyl sulfoxide (DMSO), diluted in PBS, and then intraperitoneally injected into mice at a dose of 250 mg/kg once a day.

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Response regulation Metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc-inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells.
Experiment 5 Reporting the Ferroptosis-centered Drug Act on This Target [5]
Target for Ferroptosis Suppressor
Responsed Disease Uterine serous carcinoma ICD-11: 2C72
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model hUPSCs (Human uterine serous papillary carcinoma-1 cells)
Abcam HeLa ERGIC2 KO cells Endocervical adenocarcinoma Homo sapiens CVCL_B1RG
SK-OV-3 cells Ovarian serous cystadenocarcinoma Homo sapiens CVCL_0532
In Vivo Model
The mean weight of the mice at the start was 19.4 ± 0.87 g. To generate the subcutaneous xenograft model, USPC1 (5 x 106 cells) or PTX1 (5 x 106 cells) were suspended in 200 ul of PBS following determination of cellular viability and injected into the subcutaneous tissue of 6-week-old female Crj:SHO-PrkdcscidHrhr hairless SCID mice (n = 2) (Charles River Laboratories Inc.). Tumor formation was visually confirmed in mice inoculated with USPC1 cells, but not in those inoculated with PTX1 cells, thus the animal study was performed using USPC1 cells. The recipient mice were monitored for general health status and presence of subcutaneous tumors once a week.

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Response regulation The effect of the xCT (SLC7A11) inhibitor, sulfasalazine on cytotoxicity was stronger in paclitaxel-resistant uterine serous carcinoma (USC) cells compared with that in paclitaxel-sensitive USC cells. Furthermore, the synthetic lethal interaction between the accumulation of ROS and the activation of the Ras effector, JNK, induced cell-proliferation inhibition and ferroptotic cell death in paclitaxel-resistant USC cells.
Transferrin receptor protein 1 (TFRC)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [2]
Target for Ferroptosis Marker/Suppressor/Driver
Responsed Disease Breast cancer ICD-11: 2C60
 Disease Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
T-47D cells Invasive breast carcinoma Homo sapiens CVCL_0553
BT-549 cells Invasive breast carcinoma Homo sapiens CVCL_1092
MCF-7 cells Breast carcinoma Homo sapiens CVCL_0031
Response regulation Sulfasalazine (SAS) upregulated TFRC and DMT1. Knockdown of the ER increased TFRC expression in breast cancer cells. In conclusion SAS could trigger ferroptosis in breast cancer cells, especially in cells with low ER expression.
Natural resistance-associated macrophage protein 2 (SLC11A2)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [2]
Target for Ferroptosis Driver
Responsed Disease Breast cancer ICD-11: 2C60
 Disease Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
T-47D cells Invasive breast carcinoma Homo sapiens CVCL_0553
BT-549 cells Invasive breast carcinoma Homo sapiens CVCL_1092
MCF-7 cells Breast carcinoma Homo sapiens CVCL_0031
Response regulation Sulfasalazine (SAS) upregulated TFRC and DMT1. Knockdown of the ER increased TFRC expression in breast cancer cells. In conclusion SAS could trigger ferroptosis in breast cancer cells, especially in cells with low ER expression.
Beclin-1 (BECN1)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Colon cancer ICD-11: 2B90
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
AMPK signaling pathway hsa04152
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model HCT 116 cells Colon carcinoma Homo sapiens CVCL_0291
PANC-1 cells Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Calu-1 cells Lung squamous cell carcinoma Homo sapiens CVCL_0608
HeLa cells Endocervical adenocarcinoma Homo sapiens CVCL_0030
HEK-293T cells Normal Homo sapiens CVCL_0063
In Vivo Model
To generate murine subcutaneous tumors, 5 x 106 HCT116, CX-1, or HT1080 cells in 100 ul phosphate buffered saline (PBS; Thermo Fisher Scientific, AM9625) were injected subcutaneously right of the dorsal midline in athymic nude immunodeficient mice (six- to eight-week-old, female). To generate orthotopic tumors, 1 x 106 KPC cells in 10 ul PBS were surgically implanted into the pancreases of immunocompetent C57BL/6J mice (six- to eight-week-old, female).

    Click to Show/Hide
Response regulation BECN1 plays a novel role in lipid peroxidation that could be exploited to improve anticancer therapy by the induction of ferroptosis in Colon cancer. Mechanistically, phosphorylation of BECN1 at Ser90/93/96 by PRKAA/AMPK contributes to the formation of a BECN1-SLC7A11 complex and system Xc-inhibition. Knockdown of BECN1 by shRNA inhibits ferroptosis induced by system X-c- inhibitors (e.g., erastin, sulfasalazine, and sorafenib).
References
Ref 1 AMPK-Mediated BECN1 Phosphorylation Promotes Ferroptosis by Directly Blocking System X(c)(-) Activity. Curr Biol. 2018 Aug 6;28(15):2388-2399.e5. doi: 10.1016/j.cub.2018.05.094. Epub 2018 Jul 26.
Ref 2 Sulfasalazineinduced ferroptosis in breast cancer cells is reduced by the inhibitory effect of estrogen receptor on the transferrin receptor. Oncol Rep. 2019 Aug;42(2):826-838. doi: 10.3892/or.2019.7189. Epub 2019 Jun 6.
Ref 3 xCT Inhibition Increases Sensitivity to Vorinostat in a ROS-Dependent Manner. Cancers (Basel). 2020 Mar 30;12(4):827. doi: 10.3390/cancers12040827.
Ref 4 Metformin induces Ferroptosis by inhibiting UFMylation of SLC7A11 in breast cancer. J Exp Clin Cancer Res. 2021 Jun 23;40(1):206. doi: 10.1186/s13046-021-02012-7.
Ref 5 xCT inhibitor sulfasalazine depletes paclitaxel-resistant tumor cells through ferroptosis in uterine serous carcinoma. Oncol Lett. 2020 Sep;20(3):2689-2700. doi: 10.3892/ol.2020.11813. Epub 2020 Jul 6.