Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10047)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
AQP8
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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Cytochrome b-245 heavy chain (CYBB) [Driver]
In total 2 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5, AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 2 Reporting the Ferroptosis Target of This Regulator | [1] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Cervical cancer [ICD-11: 2C77]
In total 2 item(s) under this disease | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | |||
Target Regulator | Aquaporin-8 (AQP8) | Protein coding | ||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5, AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 2 Reporting the Ferroptosis-centered Disease Response | [1] | |||
Target Regulator | Aquaporin-8 (AQP8) | Protein coding | ||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Hydrogen Peroxide
[Investigative]
In total 2 item(s) under this drug | ||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | |||
Drug for Ferroptosis | Inducer | |||
Response Target | Cytochrome b-245 heavy chain (CYBB) | Driver | ||
Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5, AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 2 Reporting the Ferroptosis-centered Drug Response | [1] | |||
Drug for Ferroptosis | Inducer | |||
Response Target | Cytochrome b-245 heavy chain (CYBB) | Driver | ||
Responsed Disease | Cervical cancer | ICD-11: 2C77 | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||