Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10058)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
KRAS
can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
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Unspecific Target [Unspecific Target]
In total 2 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | |||
Responsed Disease | Lung cancer | ICD-11: 2C25 | ||
Responsed Drug | Tetraarsenic tetrasulfide | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
MAPK signaling pathway | hsa04010 | |||
Apoptosis | hsa04210 | |||
Cell Process | Cell ferroptosis | |||
Cell apoptosis | ||||
Cell proliferation | ||||
In Vitro Model |
NCI-H23 cells | Lung adenocarcinoma | Homo sapiens | CVCL_1547 |
A-549 cells | Lung adenocarcinoma | Homo sapiens | CVCL_0023 | |
NCI-H460 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0459 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | |
Response regulation | Realgar-induced ferroptosis may be mediated via KRAS/Raf/MAPK. Realgar may be targeted to regulate Raf kinase, thereby further regulating the downstream JNK/ERK signaling cascade to suppress KRAS cells and exert an anticancer activity. In conclusion, realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer. | |||
Experiment 2 Reporting the Ferroptosis Target of This Regulator | [2] | |||
Responsed Disease | Rhabdomyosarcoma | ICD-11: 2B55 | ||
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). | |||
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | |||
Target Regulator | GTPase KRas (KRAS) | Protein coding | ||
Responsed Drug | Tetraarsenic tetrasulfide | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
MAPK signaling pathway | hsa04010 | |||
Apoptosis | hsa04210 | |||
Cell Process | Cell ferroptosis | |||
Cell apoptosis | ||||
Cell proliferation | ||||
In Vitro Model |
NCI-H23 cells | Lung adenocarcinoma | Homo sapiens | CVCL_1547 |
A-549 cells | Lung adenocarcinoma | Homo sapiens | CVCL_0023 | |
NCI-H460 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0459 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | |
Response regulation | Realgar-induced ferroptosis may be mediated via KRAS/Raf/MAPK. Realgar may be targeted to regulate Raf kinase, thereby further regulating the downstream JNK/ERK signaling cascade to suppress KRAS cells and exert an anticancer activity. In conclusion, realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer. | |||
Rhabdomyosarcoma [ICD-11: 2B55]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | |||
Target Regulator | GTPase KRas (KRAS) | Protein coding | ||
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). | |||
Tetraarsenic tetrasulfide
[Investigative]
In total 1 item(s) under this drug | ||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | |||
Drug for Ferroptosis | Inducer | |||
Response Target | Unspecific Target | |||
Responsed Disease | Lung cancer | ICD-11: 2C25 | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
MAPK signaling pathway | hsa04010 | |||
Apoptosis | hsa04210 | |||
Cell Process | Cell ferroptosis | |||
Cell apoptosis | ||||
Cell proliferation | ||||
In Vitro Model |
NCI-H23 cells | Lung adenocarcinoma | Homo sapiens | CVCL_1547 |
A-549 cells | Lung adenocarcinoma | Homo sapiens | CVCL_0023 | |
NCI-H460 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0459 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | |
Response regulation | Realgar-induced ferroptosis may be mediated via KRAS/Raf/MAPK. Realgar may be targeted to regulate Raf kinase, thereby further regulating the downstream JNK/ERK signaling cascade to suppress KRAS cells and exert an anticancer activity. In conclusion, realgar may induce ferroptosis by regulating the Raf, and hence plays a role in antiKRAS mutant lung cancer. | |||
References