Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10076)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
JUN
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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Nuclear receptor coactivator 4 (NCOA4) [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 | Degenerative arthritis | ICD-11: FA05 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Autophagy | hsa04140 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell autophagy | |||||
In Vitro Model |
hCDs (Chondrocytes) | ||||
| In Vivo Model |
Adult male C57BL/6 mice (eight weeks of age) were used for in vivo experiments. We randomly divided mice into four groups with 9 mice per group: SHAM + AAV9-GFP, SHAM + AAV9-NCOA4, DMM + AAV9-GFP, and DMM + AAV9-NCOA4 groups. For in vivo experiment of SP600125 administration, we randomly divided mice into three groups with 6 mice per group: DMM + AAV9-GFP, DMM + AAV9-GFP + SP600125, and DMM + AAV9-NCOA4 + SP600125. 10 ul of SP600125 (1 mg/kg) or vehicle solution was injected articularly once per week for 7 weeks.
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| Response regulation | NCOA4 was upregulated in a JNK- JUN signaling-dependent manner in which JUN could directly bind to the promoter of Ncoa4 and initial the transcription of Ncoa4. This work highlights the role of JNK- JUN-NCOA4 axis and ferritinophagy in chondrocyte ferroptosis and osteoarthritis (OA) pathogenesis, suggesting this axis as a potential target for OA treatment. | ||||
Unspecific Target [Unspecific Target]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
| Responsed Disease | Hepatocellular carcinoma | ICD-11: 2C12 | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
BEL-7402 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_5492 | |
| SMMC-7721 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0534 | ||
| In Vivo Model |
Eight-week-old athymic nude mice were obtained from Bikai Laboratory Animal Crop (Bikai, Shanghai, China) and Bel-7402 cells (initial 5 x 106) were subcutaneously injected into each mouse. Dimethy sulfoxide (DMSO) or piperazine erastin (5 mg/kg, MedChemExpress, Monmouth Junction, NJ, USA) was subcutaneously injected once every day after xenografts were formed.
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| Response regulation | A positive correlation between c-Jun O-GlcNAcylation and GSH was observed in clinical samples. Collectively, O-GlcNAcylated c-Jun represents an obstructive factor to ferroptosis, and targeting O-GlcNAcylated c-Jun might be helpful for treating liver cancer. | ||||
Degenerative arthritis [ICD-11: FA05]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | Transcription factor Jun (JUN) | Protein coding | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Autophagy | hsa04140 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell autophagy | |||||
In Vitro Model |
hCDs (Chondrocytes) | ||||
| In Vivo Model |
Adult male C57BL/6 mice (eight weeks of age) were used for in vivo experiments. We randomly divided mice into four groups with 9 mice per group: SHAM + AAV9-GFP, SHAM + AAV9-NCOA4, DMM + AAV9-GFP, and DMM + AAV9-NCOA4 groups. For in vivo experiment of SP600125 administration, we randomly divided mice into three groups with 6 mice per group: DMM + AAV9-GFP, DMM + AAV9-GFP + SP600125, and DMM + AAV9-NCOA4 + SP600125. 10 ul of SP600125 (1 mg/kg) or vehicle solution was injected articularly once per week for 7 weeks.
Click to Show/Hide
|
||||
| Response regulation | NCOA4 was upregulated in a JNK- JUN signaling-dependent manner in which JUN could directly bind to the promoter of Ncoa4 and initial the transcription of Ncoa4. This work highlights the role of JNK- JUN-NCOA4 axis and ferritinophagy in chondrocyte ferroptosis and osteoarthritis (OA) pathogenesis, suggesting this axis as a potential target for OA treatment. | ||||
Hepatocellular carcinoma [ICD-11: 2C12]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
| Target Regulator | Transcription factor Jun (JUN) | Protein coding | |||
| Pathway Response | Ferroptosis | hsa04216 | |||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
BEL-7402 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_5492 | |
| SMMC-7721 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0534 | ||
| In Vivo Model |
Eight-week-old athymic nude mice were obtained from Bikai Laboratory Animal Crop (Bikai, Shanghai, China) and Bel-7402 cells (initial 5 x 106) were subcutaneously injected into each mouse. Dimethy sulfoxide (DMSO) or piperazine erastin (5 mg/kg, MedChemExpress, Monmouth Junction, NJ, USA) was subcutaneously injected once every day after xenografts were formed.
Click to Show/Hide
|
||||
| Response regulation | A positive correlation between c-Jun O-GlcNAcylation and GSH was observed in clinical samples. Collectively, O-GlcNAcylated c-Jun represents an obstructive factor to ferroptosis, and targeting O-GlcNAcylated c-Jun might be helpful for treating liver cancer. | ||||
References