Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10054)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
EGFR
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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Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Lung cancer | ICD-11: 2C25 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
hTERT-HME1 cells | Normal | Homo sapiens | CVCL_3383 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | ||
In Vivo Model |
2.5 x 105 NCI-H1650 cells were inoculated 1:1 in Matrigel: PBS (100 mL) by subcutaneous injection into eight non-obese diabetic (NOD) severe combined immunodeficiency (SCID) gamma male mice. Tumors were allowed to engraft and grow for 30 days (tumor volume averaged ~200 mm3) and mice treated by intraperitoneal (i.p.) injection with 100 mg/kg cyst(e)inase or 100 mg/kg heat-inactivated cyst(e)inase (n = 4 ea.) on day 30, with a second dose given on day 33. Mice were necropsied 24 hr after the second dose.
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Response regulation | In non-small-cell lung cancer (NSCLC) cells, active MAPK signaling downstream of active EGFR can sensitize cells to ferroptosis upon cystine depletion. Sensitization involves both impaired detoxification of lipid peroxides, due to reduced expression of GPX4, and generation of hydrogen peroxide, via NOX4. | ||||
NADPH oxidase 4 (NOX4) [Driver]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Lung cancer | ICD-11: 2C25 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
hTERT-HME1 cells | Normal | Homo sapiens | CVCL_3383 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | ||
In Vivo Model |
2.5 x 105 NCI-H1650 cells were inoculated 1:1 in Matrigel: PBS (100 mL) by subcutaneous injection into eight non-obese diabetic (NOD) severe combined immunodeficiency (SCID) gamma male mice. Tumors were allowed to engraft and grow for 30 days (tumor volume averaged ~200 mm3) and mice treated by intraperitoneal (i.p.) injection with 100 mg/kg cyst(e)inase or 100 mg/kg heat-inactivated cyst(e)inase (n = 4 ea.) on day 30, with a second dose given on day 33. Mice were necropsied 24 hr after the second dose.
Click to Show/Hide
|
||||
Response regulation | In non-small-cell lung cancer (NSCLC) cells, active MAPK signaling downstream of active EGFR can sensitize cells to ferroptosis upon cystine depletion. Sensitization involves both impaired detoxification of lipid peroxides, due to reduced expression of GPX4, and generation of hydrogen peroxide, via NOX4. | ||||
Lung cancer [ICD-11: 2C25]
In total 2 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Epidermal growth factor receptor (EGFR) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
hTERT-HME1 cells | Normal | Homo sapiens | CVCL_3383 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | ||
In Vivo Model |
2.5 x 105 NCI-H1650 cells were inoculated 1:1 in Matrigel: PBS (100 mL) by subcutaneous injection into eight non-obese diabetic (NOD) severe combined immunodeficiency (SCID) gamma male mice. Tumors were allowed to engraft and grow for 30 days (tumor volume averaged ~200 mm3) and mice treated by intraperitoneal (i.p.) injection with 100 mg/kg cyst(e)inase or 100 mg/kg heat-inactivated cyst(e)inase (n = 4 ea.) on day 30, with a second dose given on day 33. Mice were necropsied 24 hr after the second dose.
Click to Show/Hide
|
||||
Response regulation | In non-small-cell lung cancer (NSCLC) cells, active MAPK signaling downstream of active EGFR can sensitize cells to ferroptosis upon cystine depletion. Sensitization involves both impaired detoxification of lipid peroxides, due to reduced expression of GPX4, and generation of hydrogen peroxide, via NOX4. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Epidermal growth factor receptor (EGFR) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
hTERT-HME1 cells | Normal | Homo sapiens | CVCL_3383 | |
H1650-ER1 cells | Minimally invasive lung adenocarcinoma | Homo sapiens | CVCL_4V01 | ||
In Vivo Model |
2.5 x 105 NCI-H1650 cells were inoculated 1:1 in Matrigel: PBS (100 mL) by subcutaneous injection into eight non-obese diabetic (NOD) severe combined immunodeficiency (SCID) gamma male mice. Tumors were allowed to engraft and grow for 30 days (tumor volume averaged ~200 mm3) and mice treated by intraperitoneal (i.p.) injection with 100 mg/kg cyst(e)inase or 100 mg/kg heat-inactivated cyst(e)inase (n = 4 ea.) on day 30, with a second dose given on day 33. Mice were necropsied 24 hr after the second dose.
Click to Show/Hide
|
||||
Response regulation | In non-small-cell lung cancer (NSCLC) cells, active MAPK signaling downstream of active EGFR can sensitize cells to ferroptosis upon cystine depletion. Sensitization involves both impaired detoxification of lipid peroxides, due to reduced expression of GPX4, and generation of hydrogen peroxide, via NOX4. | ||||