Ferroptosis-centered Disease Response Information

General Information of the Disease (ID: DIS00020)
Name
Rhabdomyosarcoma
ICD
ICD-11: 2B55
Full List of Target(s) of This Ferroptosis-centered Disease
Unspecific Target
In total 9 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Bisindolylmaleimide i Investigative
 Drug Info 
Responsed Regulator Protein kinase C alpha type (PRKCA) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a (PRKCA) and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Responsed Regulator Dual oxidase 2 (DUOX2) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Responsed Regulator Dual oxidase 1 (DUOX1) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 4 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Responsed Regulator NADPH oxidase 3 (NOX3) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 5 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Responsed Regulator NADPH oxidase 5 (NOX5) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 6 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Go-6976 Investigative
 Drug Info 
Responsed Regulator Protein kinase C alpha type (PRKCA) Driver
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a (PRKCA) and b-selective inhibitor Go-6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 7 Reporting the Ferroptosis-centered Disease Response by This Target [2]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Regulator GTPase HRas (HRAS) Driver
 Regulator Info 
Pathway Response Ferroptosis hsa04216
MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
Cell proliferation
In Vitro Model RMS13 cells Rhabdomyosarcoma Mus musculus CVCL_S112
Response regulation Oncogenic RAS ( HRAS, NRAS, KRAS) selectively modulates cell death pathways triggered by cytotoxic stimuli in rhabdomyosarcoma RMS13 cells. In conclusion, our discovery of an increased resistance to oxidative stress imposed by oncogenic RAS mutants in RMS13 cells has important implications for the development of targeted therapies for rhabdomyosarcoma (RMS).
Experiment 8 Reporting the Ferroptosis-centered Disease Response by This Target [2]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Regulator GTPase NRas (NRAS) Driver
 Regulator Info 
Pathway Response Ferroptosis hsa04216
MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
Cell proliferation
In Vitro Model RMS13 cells Rhabdomyosarcoma Mus musculus CVCL_S112
Response regulation Oncogenic RAS (HRAS, NRAS, KRAS) selectively modulates cell death pathways triggered by cytotoxic stimuli in rhabdomyosarcoma RMS13 cells. In conclusion, our discovery of an increased resistance to oxidative stress imposed by oncogenic RAS mutants in RMS13 cells has important implications for the development of targeted therapies for rhabdomyosarcoma (RMS).
Experiment 9 Reporting the Ferroptosis-centered Disease Response by This Target [2]
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Regulator GTPase KRas (KRAS) Driver
 Regulator Info 
Pathway Response Ferroptosis hsa04216
MAPK signaling pathway hsa04010
PI3K-Akt signaling pathway hsa04151
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
Cell proliferation
In Vitro Model RMS13 cells Rhabdomyosarcoma Mus musculus CVCL_S112
Response regulation Oncogenic RAS (HRAS, NRAS, KRAS) selectively modulates cell death pathways triggered by cytotoxic stimuli in rhabdomyosarcoma RMS13 cells. In conclusion, our discovery of an increased resistance to oxidative stress imposed by oncogenic RAS mutants in RMS13 cells has important implications for the development of targeted therapies for rhabdomyosarcoma (RMS).
NADPH oxidase 4 (NOX4)
 Target Info 
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Driver
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug GKT137831 Phase 2
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Driver
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
NADPH oxidase 1 (NOX1)
 Target Info 
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Driver
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug GKT137831 Phase 2
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Driver
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC- and -selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX) inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
Cytochrome b-245 heavy chain (CYBB)
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Driver
Responsed Disease Rhabdomyosarcoma [ICD-11: 2B55]
Responsed Drug Diphenyleneiodonium Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model RD cells Rhabdomyosarcoma Homo sapiens CVCL_1649
Rh18 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_1659
Rh30 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_0041
Rh36 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_M599
Rh41 cells Alveolar rhabdomyosarcoma Homo sapiens CVCL_2176
T 174 cells Rhabdomyosarcoma Homo sapiens CVCL_U955
TE 381.T cells Rhabdomyosarcoma Homo sapiens CVCL_1751
KYM-1 cells Embryonal rhabdomyosarcoma Homo sapiens CVCL_3007
Response regulation Rhabdomyosarcoma (RMS) cells might be vulnerable to oxidative stress-induced cell death. The broad-spectrum protein kinase C (PKC) inhibitor Bisindolylmaleimide I as well as the PKC-a and b-selective inhibitor G6976 significantly reduced Erastin-induced cell death. Furthermore, the broad-spectrum nicotinamide adenine dinucleotide phosphate-oxidase (NOX, including NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2 inhibitor Diphenyleneiodonium and the selective NOX1/4 isoform inhibitor GKT137831 significantly decreased Erastin-stimulated ROS, lipid ROS and cell death.
References
Ref 1 Targeting ferroptosis in rhabdomyosarcoma cells. Int J Cancer. 2020 Jan 15;146(2):510-520. doi: 10.1002/ijc.32496. Epub 2019 Jul 4.
Ref 2 Oncogenic RAS Mutants Confer Resistance of RMS13 Rhabdomyosarcoma Cells to Oxidative Stress-Induced Ferroptotic Cell Death. Front Oncol. 2015 Jun 22;5:131. doi: 10.3389/fonc.2015.00131. eCollection 2015.