Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20029)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-150-5p
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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Long-chain-fatty-acid--CoA ligase 4 (ACSL4) [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 | Colorectal cancer | ICD-11: 2B91 | |||
Responsed Drug | Bromelain | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
NCI-H508 cells | Cecum adenocarcinoma | Homo sapiens | CVCL_1564 | |
HCT 116 cells | Colon carcinoma | Homo sapiens | CVCL_0291 | ||
G13D (Human colorectal cancer cells) | |||||
DLD-1 cells | Colon adenocarcinoma | Homo sapiens | CVCL_0248 | ||
G12D (Human colorectal cancer cells) | |||||
CCD-18Co cells | Normal | Homo sapiens | CVCL_2379 | ||
In Vivo Model |
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.
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Response regulation | Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4. | ||||
Ubiquitin carboxyl-terminal hydrolase BAP1 (BAP1) [Driver]
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Parkinson disease | ICD-11: 8A00 | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
SK-N-SH cells | Neuroblastoma | Homo sapiens | CVCL_0531 |
Response regulation | Dysregulated ferroptosis is closely associated with Parkinson's disease (PD) progression. NEAT1 functioned as a sponge to suppress miR-150-5p expression. Moreover, miR-150-5p overexpression suppressed ferroptosis in PD cell model. And miR-150-5p regulated SLC7A11 expression by directly binding to BAP1. | |||
Sodium-coupled neutral amino acid symporter 1 (SLC38A1) [Driver]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [3] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Pulmonary fibrosis | ICD-11: CB03 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell migration | |||||
In Vitro Model |
HFL1 cells | Normal | Homo sapiens | CVCL_0298 | |
In Vivo Model |
Male Sprague-Dawley rats (200-220 g) were purchased from Weitonglihua Company (Beijing, China) and maintained in a pathogen-free facility. After one week of adaptive feeding, a total of 30 rats were randomly divided into 3 groups (n = 10 rats/group): a control group; bleomycin (BLM) group; and BLM + sh-ZFAS1 group. Rats in the BLM group were administered 5 mg/kg BLM (Nippon Kayaku, Japan) dissolved in phosphate buffered saline (PBS) and administered to the rats intratracheally to establish the PF model. Rats in the control group were treated with 0.05 mL PBS. Rats in the BLM + sh-ZFAS1 group were injected intraperitoneally with 30 uL lncRNA ZFAS1 shRNA adeno-associated virus 5 (Vigene Biosciences, USA) for 3 weeks prior to an injection of 5 mg/kg BLM sulfate.
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Response regulation | Inhibition of lncRNA ZFAS1 abolished BLM-induced lipid peroxidation and pulmonary fibrosis (PF) development. Mechanistically, silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression. | ||||
Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [4] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Cardiomyopathy | ICD-11: BC43 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell apoptosis | |||||
In Vitro Model |
hCMs (Human cardiomyocytes) | ||||
In Vivo Model |
To simulate the animal model of diabetic cardiomyopathy, male db/+ mice and db/db mice (age, 7 weeks, weight, 24 g) were fed a normal diet for 4 weeks and kept at 24 under a 14-h light/8-h dark cycle. The animals were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China). Diabetic mice were intracoronarily administered equal volumes (80 ul) of adenoviruses Ad-ZFAS1, Ad-sh-ZFAS1, Ad-CCND2, Ad-sh-CCND2 or Ad-NC.33 miR-150-5p mimics and mimic control (NC) were injected into the tail vein of mice (50 ug/kg) every 15 days for 12 weeks. Db/db mice were treated with or without ferrostatin-1 (Fer-1, ferroptosis inhibitor; Sigma-Aldrich, 5 mg/kg) for an additional 12 weeks.
Click to Show/Hide
|
||||
Response regulation | lncRNA-ZFAS1 acted as a ceRNA to sponge miR-150-5p and downregulate CCND2 to promote cardiomyocyte ferroptosis and Diabetic cardiomyopathy development. Inhibition of ZFAS1 restored the expression of FTH1, reduced the expression of 4HNE, rescued the expression of GPX4 and inhibited the expression of apoptosisrelated genes. | ||||
Ferritin heavy chain (FTH1) [Suppressor; Marker]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [4] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Cardiomyopathy | ICD-11: BC43 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell apoptosis | |||||
In Vitro Model |
hCMs (Human cardiomyocytes) | ||||
In Vivo Model |
To simulate the animal model of diabetic cardiomyopathy, male db/+ mice and db/db mice (age, 7 weeks, weight, 24 g) were fed a normal diet for 4 weeks and kept at 24 under a 14-h light/8-h dark cycle. The animals were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China). Diabetic mice were intracoronarily administered equal volumes (80 ul) of adenoviruses Ad-ZFAS1, Ad-sh-ZFAS1, Ad-CCND2, Ad-sh-CCND2 or Ad-NC.33 miR-150-5p mimics and mimic control (NC) were injected into the tail vein of mice (50 ug/kg) every 15 days for 12 weeks. Db/db mice were treated with or without ferrostatin-1 (Fer-1, ferroptosis inhibitor; Sigma-Aldrich, 5 mg/kg) for an additional 12 weeks.
Click to Show/Hide
|
||||
Response regulation | lncRNA-ZFAS1 acted as a ceRNA to sponge miR-150-5p and downregulate CCND2 to promote cardiomyocyte ferroptosis and Diabetic cardiomyopathy development. Inhibition of ZFAS1 restored the expression of FTH1, reduced the expression of 4HNE, rescued the expression of GPX4 and inhibited the expression of apoptosisrelated genes. | ||||
Colorectal cancer [ICD-11: 2B91]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | hsa-miR-150-5p (miRNA) | miRNA | |||
Responsed Drug | Bromelain | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
NCI-H508 cells | Cecum adenocarcinoma | Homo sapiens | CVCL_1564 | |
HCT 116 cells | Colon carcinoma | Homo sapiens | CVCL_0291 | ||
G13D (Human colorectal cancer cells) | |||||
DLD-1 cells | Colon adenocarcinoma | Homo sapiens | CVCL_0248 | ||
G12D (Human colorectal cancer cells) | |||||
CCD-18Co cells | Normal | Homo sapiens | CVCL_2379 | ||
In Vivo Model |
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.
Click to Show/Hide
|
||||
Response regulation | Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4. | ||||
Parkinson disease [ICD-11: 8A00]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | |||
Target Regulator | hsa-miR-150-5p (miRNA) | miRNA | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Cell Process | Cell ferroptosis | |||
In Vitro Model |
SK-N-SH cells | Neuroblastoma | Homo sapiens | CVCL_0531 |
Response regulation | Dysregulated ferroptosis is closely associated with Parkinson's disease (PD) progression. NEAT1 functioned as a sponge to suppress miR-150-5p expression. Moreover, miR-150-5p overexpression suppressed ferroptosis in PD cell model. And miR-150-5p regulated SLC7A11 expression by directly binding to BAP1. | |||
Cardiomyopathy [ICD-11: BC43]
In total 2 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [4] | ||||
Target Regulator | hsa-miR-150-5p (miRNA) | miRNA | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell apoptosis | |||||
In Vitro Model |
hCMs (Human cardiomyocytes) | ||||
In Vivo Model |
To simulate the animal model of diabetic cardiomyopathy, male db/+ mice and db/db mice (age, 7 weeks, weight, 24 g) were fed a normal diet for 4 weeks and kept at 24 under a 14-h light/8-h dark cycle. The animals were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China). Diabetic mice were intracoronarily administered equal volumes (80 ul) of adenoviruses Ad-ZFAS1, Ad-sh-ZFAS1, Ad-CCND2, Ad-sh-CCND2 or Ad-NC.33 miR-150-5p mimics and mimic control (NC) were injected into the tail vein of mice (50 ug/kg) every 15 days for 12 weeks. Db/db mice were treated with or without ferrostatin-1 (Fer-1, ferroptosis inhibitor; Sigma-Aldrich, 5 mg/kg) for an additional 12 weeks.
Click to Show/Hide
|
||||
Response regulation | lncRNA-ZFAS1 acted as a ceRNA to sponge miR-150-5p and downregulate CCND2 to promote cardiomyocyte ferroptosis and Diabetic cardiomyopathy development. Inhibition of ZFAS1 restored the expression of FTH1, reduced the expression of 4HNE, rescued the expression of GPX4 and inhibited the expression of apoptosisrelated genes. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response | [4] | ||||
Target Regulator | hsa-miR-150-5p (miRNA) | miRNA | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell apoptosis | |||||
In Vitro Model |
hCMs (Human cardiomyocytes) | ||||
In Vivo Model |
To simulate the animal model of diabetic cardiomyopathy, male db/+ mice and db/db mice (age, 7 weeks, weight, 24 g) were fed a normal diet for 4 weeks and kept at 24 under a 14-h light/8-h dark cycle. The animals were purchased from the Model Animal Research Center of Nanjing University (Nanjing, China). Diabetic mice were intracoronarily administered equal volumes (80 ul) of adenoviruses Ad-ZFAS1, Ad-sh-ZFAS1, Ad-CCND2, Ad-sh-CCND2 or Ad-NC.33 miR-150-5p mimics and mimic control (NC) were injected into the tail vein of mice (50 ug/kg) every 15 days for 12 weeks. Db/db mice were treated with or without ferrostatin-1 (Fer-1, ferroptosis inhibitor; Sigma-Aldrich, 5 mg/kg) for an additional 12 weeks.
Click to Show/Hide
|
||||
Response regulation | lncRNA-ZFAS1 acted as a ceRNA to sponge miR-150-5p and downregulate CCND2 to promote cardiomyocyte ferroptosis and Diabetic cardiomyopathy development. Inhibition of ZFAS1 restored the expression of FTH1, reduced the expression of 4HNE, rescued the expression of GPX4 and inhibited the expression of apoptosisrelated genes. | ||||
Pulmonary fibrosis [ICD-11: CB03]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [3] | ||||
Target Regulator | hsa-miR-150-5p (miRNA) | miRNA | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell migration | |||||
In Vitro Model |
HFL1 cells | Normal | Homo sapiens | CVCL_0298 | |
In Vivo Model |
Male Sprague-Dawley rats (200-220 g) were purchased from Weitonglihua Company (Beijing, China) and maintained in a pathogen-free facility. After one week of adaptive feeding, a total of 30 rats were randomly divided into 3 groups (n = 10 rats/group): a control group; bleomycin (BLM) group; and BLM + sh-ZFAS1 group. Rats in the BLM group were administered 5 mg/kg BLM (Nippon Kayaku, Japan) dissolved in phosphate buffered saline (PBS) and administered to the rats intratracheally to establish the PF model. Rats in the control group were treated with 0.05 mL PBS. Rats in the BLM + sh-ZFAS1 group were injected intraperitoneally with 30 uL lncRNA ZFAS1 shRNA adeno-associated virus 5 (Vigene Biosciences, USA) for 3 weeks prior to an injection of 5 mg/kg BLM sulfate.
Click to Show/Hide
|
||||
Response regulation | Inhibition of lncRNA ZFAS1 abolished BLM-induced lipid peroxidation and pulmonary fibrosis (PF) development. Mechanistically, silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression. | ||||
Bromelain
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
Drug for Ferroptosis | Inducer | ||||
Response Target | Long-chain-fatty-acid--CoA ligase 4 (ACSL4) | Driver | |||
Responsed Disease | Colorectal cancer | ICD-11: 2B91 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
NCI-H508 cells | Cecum adenocarcinoma | Homo sapiens | CVCL_1564 | |
HCT 116 cells | Colon carcinoma | Homo sapiens | CVCL_0291 | ||
G13D (Human colorectal cancer cells) | |||||
DLD-1 cells | Colon adenocarcinoma | Homo sapiens | CVCL_0248 | ||
G12D (Human colorectal cancer cells) | |||||
CCD-18Co cells | Normal | Homo sapiens | CVCL_2379 | ||
In Vivo Model |
Animals (n = 7) were given 2.5% DSS in drinking water for 5 days and then no treatment for 14 days as one cycle; this process was repeated for three cycles. In the last cycle, 2% DSS water treated to each group and no treatment for 14 days. During the three DSS cycle, 3 mg/kg bromelain were injected daily intraperitoneally and colon and spleen tissues were harvested after three DSS cycle in 57 days to study polyp burden and to perform histological staining.
Click to Show/Hide
|
||||
Response regulation | Elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2cells compared to in DLD-1 cells potentially targeted ACSL-4 and resulted in suppression of ACSL-4. Overall, bromelain inhibits proliferation of Kras mutant Colorectal Cancer (CRC) effectively via ACSL-4. | ||||
References