Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10518)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
PRNP
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
Browse Drug
Unspecific Target [Unspecific Target]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Responsed Disease | Lung cancer | ICD-11: 2C25 | |||
Responsed Drug | Borneol | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Autophagy | hsa04140 | ||||
Cell adhesion molecules | hsa04514 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
H460/CisR cells | Lung large cell carcinoma | Homo sapiens | CVCL_C5S1 | |
In Vivo Model |
Male Balb/c nude mice (4-week-old) were purchased from SPF (Beijing) biotechnology co., LTD and maintained in the Experimental Animal Research Center of Chengdu University of TCM. After 1 week of adaptable feeding, H460/CDDP cells (5 x 106 cells in 0.1 ml phosphate-buffered saline) were subcutaneously injected into the right dorsal flank to establish tumor model. When the tumor volume grows to 100 mm3, the tumor-bearing mice were randomly divided into the following four treatment groups: a control group (Con, n = 6): intraperitoneal injection of saline once a day; vehicle group (Vehicle, n = 6): intragastric administration of 2% tween and intraperitoneal injection of saline; d-borneol low-dose group (Bor-L, n = 6): intragastric administration of d-borneol (30 mg/kg) once a day; d-borneol high-dose group (Bor-H, n = 6): intragastric administration of d-borneol (60 mg/kg) once a day; CDDP group (CDDP, n = 6): intraperitoneal injection of cisplatin (3 mg/kg) every two days; a low-dose combination treatment group (C+B-L, n = 6): intragastric administration of d-borneol (30 mg/kg) once a day and intraperitoneal injection of cisplatin (3 mg/kg) every two days; a high-dose combination treatment group (C+B-H, n = 6): intragastric administration of d-borneol (60 mg/kg) once a day and intraperitoneal injection of cisplatin (3 mg/kg) every two days. We usually first orally gavage d-borneol, and then inject cisplatin intraperitoneally half an hour later. After 14 days treatment, the samples were obtained from the mice for the further experiments.
Click to Show/Hide
|
||||
Response regulation | d-borneol in combination with cisplatin induced ferroptosisvia NCOA4-mediated ferritinophagy and also increased the expression levels of ACSL4, regulated PCBP2 and PRNP to promote the conversion of Fe3+ to Fe2+, reduced the activity or expression of antioxidants enzymes (GSH and HO-1), and induced ROS accumulation and thereby promoted ferroptosis. In addition, activation of autophagy inhibited progression of the EMT and increased sensitivity to cisplatin in cisplatin-resistant lung cancer cells. | ||||
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Major prion protein (PRNP) | Protein coding | |||
Responsed Drug | Borneol | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Autophagy | hsa04140 | ||||
Cell adhesion molecules | hsa04514 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
H460/CisR cells | Lung large cell carcinoma | Homo sapiens | CVCL_C5S1 | |
In Vivo Model |
Male Balb/c nude mice (4-week-old) were purchased from SPF (Beijing) biotechnology co., LTD and maintained in the Experimental Animal Research Center of Chengdu University of TCM. After 1 week of adaptable feeding, H460/CDDP cells (5 x 106 cells in 0.1 ml phosphate-buffered saline) were subcutaneously injected into the right dorsal flank to establish tumor model. When the tumor volume grows to 100 mm3, the tumor-bearing mice were randomly divided into the following four treatment groups: a control group (Con, n = 6): intraperitoneal injection of saline once a day; vehicle group (Vehicle, n = 6): intragastric administration of 2% tween and intraperitoneal injection of saline; d-borneol low-dose group (Bor-L, n = 6): intragastric administration of d-borneol (30 mg/kg) once a day; d-borneol high-dose group (Bor-H, n = 6): intragastric administration of d-borneol (60 mg/kg) once a day; CDDP group (CDDP, n = 6): intraperitoneal injection of cisplatin (3 mg/kg) every two days; a low-dose combination treatment group (C+B-L, n = 6): intragastric administration of d-borneol (30 mg/kg) once a day and intraperitoneal injection of cisplatin (3 mg/kg) every two days; a high-dose combination treatment group (C+B-H, n = 6): intragastric administration of d-borneol (60 mg/kg) once a day and intraperitoneal injection of cisplatin (3 mg/kg) every two days. We usually first orally gavage d-borneol, and then inject cisplatin intraperitoneally half an hour later. After 14 days treatment, the samples were obtained from the mice for the further experiments.
Click to Show/Hide
|
||||
Response regulation | d-borneol in combination with cisplatin induced ferroptosisvia NCOA4-mediated ferritinophagy and also increased the expression levels of ACSL4, regulated PCBP2 and PRNP to promote the conversion of Fe3+ to Fe2+, reduced the activity or expression of antioxidants enzymes (GSH and HO-1), and induced ROS accumulation and thereby promoted ferroptosis. In addition, activation of autophagy inhibited progression of the EMT and increased sensitivity to cisplatin in cisplatin-resistant lung cancer cells. | ||||
Borneol
[Investigative]
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 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Autophagy | hsa04140 | ||||
Cell adhesion molecules | hsa04514 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model |
H460/CisR cells | Lung large cell carcinoma | Homo sapiens | CVCL_C5S1 | |
In Vivo Model |
Male Balb/c nude mice (4-week-old) were purchased from SPF (Beijing) biotechnology co., LTD and maintained in the Experimental Animal Research Center of Chengdu University of TCM. After 1 week of adaptable feeding, H460/CDDP cells (5 x 106 cells in 0.1 ml phosphate-buffered saline) were subcutaneously injected into the right dorsal flank to establish tumor model. When the tumor volume grows to 100 mm3, the tumor-bearing mice were randomly divided into the following four treatment groups: a control group (Con, n = 6): intraperitoneal injection of saline once a day; vehicle group (Vehicle, n = 6): intragastric administration of 2% tween and intraperitoneal injection of saline; d-borneol low-dose group (Bor-L, n = 6): intragastric administration of d-borneol (30 mg/kg) once a day; d-borneol high-dose group (Bor-H, n = 6): intragastric administration of d-borneol (60 mg/kg) once a day; CDDP group (CDDP, n = 6): intraperitoneal injection of cisplatin (3 mg/kg) every two days; a low-dose combination treatment group (C+B-L, n = 6): intragastric administration of d-borneol (30 mg/kg) once a day and intraperitoneal injection of cisplatin (3 mg/kg) every two days; a high-dose combination treatment group (C+B-H, n = 6): intragastric administration of d-borneol (60 mg/kg) once a day and intraperitoneal injection of cisplatin (3 mg/kg) every two days. We usually first orally gavage d-borneol, and then inject cisplatin intraperitoneally half an hour later. After 14 days treatment, the samples were obtained from the mice for the further experiments.
Click to Show/Hide
|
||||
Response regulation | d-borneol in combination with cisplatin induced ferroptosisvia NCOA4-mediated ferritinophagy and also increased the expression levels of ACSL4, regulated PCBP2 and PRNP to promote the conversion of Fe3+ to Fe2+, reduced the activity or expression of antioxidants enzymes (GSH and HO-1), and induced ROS accumulation and thereby promoted ferroptosis. In addition, activation of autophagy inhibited progression of the EMT and increased sensitivity to cisplatin in cisplatin-resistant lung cancer cells. | ||||