Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10202)
Regulator Name Peroxiredoxin-1 (PRDX1)
Synonyms
PAGA, PAGB, TDPX2; Natural killer cell-enhancing factor A; Proliferation-associated gene protein; Thioredoxin peroxidase 2; Thioredoxin-dependent peroxide reductase 2; Thioredoxin-dependent peroxiredoxin 1
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Gene Name PRDX1
Gene ID 5052
Regulator Type Protein coding
Uniprot ID Q06830
Sequence
MSSGNAKIGHPAPNFKATAVMPDGQFKDISLSDYKGKYVVFFFYPLDFTFVCPTEIIAFS
DRAEEFKKLNCQVIGASVDSHFCHLAWVNTPKKQGGLGPMNIPLVSDPKRTIAQDYGVLK
ADEGISFRGLFIIDDKGILRQITVNDLPVGRSVDETLRLVQAFQFTDKHGEVCPAGWKPG
SDTIKPDVQKSKEYFSKQK

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Family Peroxiredoxin family
Function
Thiol-specific peroxidase that catalyzes the reduction of hydrogen peroxide and organic hydroperoxides to water and alcohols, respectively. Plays a role in cell protection against oxidative stress by detoxifying peroxides and as sensor of hydrogen peroxide-mediated signaling events. Might participate in the signaling cascades of growth factors and tumor necrosis factor-alpha by regulating the intracellular concentrations of H(2)O(2). Reduces an intramolecular disulfide bond in GDPD5 that gates the ability to GDPD5 to drive postmitotic motor neuron differentiation.

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HGNC ID
HGNC:9352
KEGG ID hsa:5052
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
PRDX1 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).
Browse Target
Browse Disease
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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
 Disease Info 
Responsed Drug 11-hydroxy-ent-16-kaurene-15-one Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 A-549 cells Lung adenocarcinoma Homo sapiens CVCL_0023
Hep-G2 cells Hepatoblastoma Homo sapiens CVCL_0027
786-O cells Renal cell carcinoma Homo sapiens CVCL_1051
HBE1 cells Normal Homo sapiens CVCL_0287
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
HUVECs (Human umbilical vein endothelial cells)
In Vivo Model
Thirty male athymic (Balb/c-nu) mice (4-week-old) were purchased from the SPF (Beijing) biotechnology (Beijing, China) and allowed to acclimatize for 1 week. A549/CDDP cells (5 x 106 cells) were injected subcutaneously into the right anterior flanks of the mice. Two weeks after the injection of cells, when the tumors became palpable (around 100 mm3), mice were randomly divided into four groups (n = 6 per group). Tumor-bearing mice were received equal amount of solvent, CDDP (4 mg/kg) or compound 23 (10 mg/kg) or combination CDDP and 23 were injected via intraperitoneal injection. Administration was performed every 3 days for 30 days.

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Response regulation 11-hydroxy-ent-16-kaurene-15-one possessed strong inhibitory activity against several cancer cell lines. Moreover, compound 23 induced both apoptosis and ferroptosis through increasing cellular ROS levels in HepG2 cells. ROS accumulation induced by compound 23 was caused by inhibition of antioxidant systems through targeting peroxiredoxin I (Prdx I) and depletion of GSH in lung adenocarcinoma cells.
Experiment 2 Reporting the Ferroptosis Target of This Regulator [2]
Responsed Disease Fuchs endothelial corneal dystrophy ICD-11: 9A70
 Disease Info 
Responsed Drug Cumene hydroperoxide Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 hPCECs (Human primary corneal endothelial cells)
B4G12-CEnC (Human corneal endothelial cells)
HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Response regulation Cumene hydroperoxide strongly induces lipid peroxidation. Moreover, this can be suppressed by Fer-1 as well as iron chelators such as DFO (not shown). Increased oxidative stress drives the loss of PRDX1 expression and renders CEnCs susceptible to lipid peroxidation in Fuchs' endothelial corneal dystrophy.
Lung cancer [ICD-11: 2C25]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Peroxiredoxin-1 (PRDX1) Protein coding
 Regulator Info 
Responsed Drug 11-hydroxy-ent-16-kaurene-15-one Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 A-549 cells Lung adenocarcinoma Homo sapiens CVCL_0023
Hep-G2 cells Hepatoblastoma Homo sapiens CVCL_0027
786-O cells Renal cell carcinoma Homo sapiens CVCL_1051
HBE1 cells Normal Homo sapiens CVCL_0287
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
HUVECs (Human umbilical vein endothelial cells)
In Vivo Model
Thirty male athymic (Balb/c-nu) mice (4-week-old) were purchased from the SPF (Beijing) biotechnology (Beijing, China) and allowed to acclimatize for 1 week. A549/CDDP cells (5 x 106 cells) were injected subcutaneously into the right anterior flanks of the mice. Two weeks after the injection of cells, when the tumors became palpable (around 100 mm3), mice were randomly divided into four groups (n = 6 per group). Tumor-bearing mice were received equal amount of solvent, CDDP (4 mg/kg) or compound 23 (10 mg/kg) or combination CDDP and 23 were injected via intraperitoneal injection. Administration was performed every 3 days for 30 days.

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Response regulation 11-hydroxy-ent-16-kaurene-15-one possessed strong inhibitory activity against several cancer cell lines. Moreover, compound 23 induced both apoptosis and ferroptosis through increasing cellular ROS levels in HepG2 cells. ROS accumulation induced by compound 23 was caused by inhibition of antioxidant systems through targeting peroxiredoxin I (Prdx I) and depletion of GSH in lung adenocarcinoma cells.
Fuchs endothelial corneal dystrophy [ICD-11: 9A70]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator Peroxiredoxin-1 (PRDX1) Protein coding
 Regulator Info 
Responsed Drug Cumene hydroperoxide Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 hPCECs (Human primary corneal endothelial cells)
B4G12-CEnC (Human corneal endothelial cells)
HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Response regulation Cumene hydroperoxide strongly induces lipid peroxidation. Moreover, this can be suppressed by Fer-1 as well as iron chelators such as DFO (not shown). Increased oxidative stress drives the loss of PRDX1 expression and renders CEnCs susceptible to lipid peroxidation in Fuchs' endothelial corneal dystrophy.
11-hydroxy-ent-16-kaurene-15-one [Investigative]
 Drug Info 
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
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Apoptosis hsa04210
Cell Process Cell ferroptosis
Cell apoptosis
In Vitro Model
 A-549 cells Lung adenocarcinoma Homo sapiens CVCL_0023
Hep-G2 cells Hepatoblastoma Homo sapiens CVCL_0027
786-O cells Renal cell carcinoma Homo sapiens CVCL_1051
HBE1 cells Normal Homo sapiens CVCL_0287
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
HUVECs (Human umbilical vein endothelial cells)
In Vivo Model
Thirty male athymic (Balb/c-nu) mice (4-week-old) were purchased from the SPF (Beijing) biotechnology (Beijing, China) and allowed to acclimatize for 1 week. A549/CDDP cells (5 x 106 cells) were injected subcutaneously into the right anterior flanks of the mice. Two weeks after the injection of cells, when the tumors became palpable (around 100 mm3), mice were randomly divided into four groups (n = 6 per group). Tumor-bearing mice were received equal amount of solvent, CDDP (4 mg/kg) or compound 23 (10 mg/kg) or combination CDDP and 23 were injected via intraperitoneal injection. Administration was performed every 3 days for 30 days.

    Click to Show/Hide
Response regulation 11-hydroxy-ent-16-kaurene-15-one possessed strong inhibitory activity against several cancer cell lines. Moreover, compound 23 induced both apoptosis and ferroptosis through increasing cellular ROS levels in HepG2 cells. ROS accumulation induced by compound 23 was caused by inhibition of antioxidant systems through targeting peroxiredoxin I (Prdx I) and depletion of GSH in lung adenocarcinoma cells.
Cumene hydroperoxide [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [2]
Drug for Ferroptosis Inducer
Response Target Unspecific Target
Responsed Disease Fuchs endothelial corneal dystrophy ICD-11: 9A70
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 hPCECs (Human primary corneal endothelial cells)
B4G12-CEnC (Human corneal endothelial cells)
HT-1080 cells Fibrosarcoma Homo sapiens CVCL_0317
Response regulation Cumene hydroperoxide strongly induces lipid peroxidation. Moreover, this can be suppressed by Fer-1 as well as iron chelators such as DFO (not shown). Increased oxidative stress drives the loss of PRDX1 expression and renders CEnCs susceptible to lipid peroxidation in Fuchs' endothelial corneal dystrophy.
References
Ref 1 ent-Kaurane diterpenoids induce apoptosis and ferroptosis through targeting redox resetting to overcome cisplatin resistance. Redox Biol. 2021 Jul;43:101977. doi: 10.1016/j.redox.2021.101977. Epub 2021 Apr 16.
Ref 2 Peroxiredoxin-1 regulates lipid peroxidation in corneal endothelial cells. Redox Biol. 2020 Feb;30:101417. doi: 10.1016/j.redox.2019.101417. Epub 2019 Dec 30.