Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20008)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-93-5p
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 | Ovarian dysfunction | ICD-11: 5A80 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| NF-kappa B signaling pathway | hsa04064 | ||||
| Apoptosis | hsa04210 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell apoptosis | |||||
| Cell proliferation | |||||
In Vitro Model |
KGN cells | Ovarian granulosa cell tumor | Homo sapiens | CVCL_0375 | |
| In Vivo Model |
C57BL/6 J (3-week-old) female mice, weighing 15-20 g, were purchased from Beijing Vitalriver Laboratory Animal Technology Co Ltd., China. Experimental animals were randomly divided into control (glycerol treatment) and experimental groups (PCOS, DHEA treatment). The modeling method was as described previously. The PCOS model and control was verified successfully as our previous results, and ovarian tissue was extracted for RT-qPCR detection.
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| Response regulation | The overexpression of miR-93-5p can promote apoptosis by reducing the expression of Bcl2 and increasing ferroptosis by downregulating GPX4, SLC7A11 and Nrf2 expression in the KGN cell line. miR-93-5p promotes the apoptosis and ferroptosis in GC by regulating the NF-kB signaling pathway. Our study identified miR-93-5p as a new molecular target for improving the function of GCs in polycystic ovary syndrome patients. | ||||
Ovarian dysfunction [ICD-11: 5A80]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | hsa-miR-93-5p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| NF-kappa B signaling pathway | hsa04064 | ||||
| Apoptosis | hsa04210 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell apoptosis | |||||
| Cell proliferation | |||||
In Vitro Model |
KGN cells | Ovarian granulosa cell tumor | Homo sapiens | CVCL_0375 | |
| In Vivo Model |
C57BL/6 J (3-week-old) female mice, weighing 15-20 g, were purchased from Beijing Vitalriver Laboratory Animal Technology Co Ltd., China. Experimental animals were randomly divided into control (glycerol treatment) and experimental groups (PCOS, DHEA treatment). The modeling method was as described previously. The PCOS model and control was verified successfully as our previous results, and ovarian tissue was extracted for RT-qPCR detection.
Click to Show/Hide
|
||||
| Response regulation | The overexpression of miR-93-5p can promote apoptosis by reducing the expression of Bcl2 and increasing ferroptosis by downregulating GPX4, SLC7A11 and Nrf2 expression in the KGN cell line. miR-93-5p promotes the apoptosis and ferroptosis in GC by regulating the NF-kB signaling pathway. Our study identified miR-93-5p as a new molecular target for improving the function of GCs in polycystic ovary syndrome patients. | ||||