Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20003)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-19b-3p
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 2 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. | ||||
Experiment 2 Reporting the Ferroptosis Target of This Regulator | [4] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Health | ICD-11: N.A. | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
HUVECs (Human umbilical vein endothelial cells) | ||||
Response regulation | The upregulated expression of individual miRNAs, miR-17, miR-18a, miR-19a, miR-20a, miR-19b and miR-92 were determined by qRT-PCR. This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis. | ||||
Ferritin heavy chain (FTH1) [Suppressor; Marker]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [2] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Lung cancer | ICD-11: 2C25 | |||
Responsed Drug | Curcumenol | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
NCI-H1299 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0060 | |
NCI-H460 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0459 | ||
HEK-293T cells | Normal | Homo sapiens | CVCL_0063 | ||
CCD-19Lu cells | Normal | Homo sapiens | CVCL_2382 | ||
BEAS-2B cells | Normal | Homo sapiens | CVCL_0168 | ||
In Vivo Model |
A subcutaneous tumor-bearing nude mouse model was established by injecting the flank of BALB/c nude mice with 5 x 106 H460 cells. Ten days later, mice were blindly randomized into four groups and intravenously injected with 200 ul ddH2O containing 0.1% CMC-Na and 1% Tween 80, iron chelators DFO (100 mg/kg/day), curcumenol (200 mg/kg/day), and curcumenol combine DFO. Tumor long diameter, short diameter, and body weight were detected every two days after the first drug treatment. The tumor volume calculation formula: (tumor long diameter x tumor short diameter2)/2. Finally, mice were sacrificed. All tumors were collected for immunohistochemical (IHC) staining.
Click to Show/Hide
|
||||
Response regulation | The natural product curcumenol exerted its antitumor effects on lung cancer by triggering ferroptosis, and the lncRNA H19/miR-19b-3p/FTH1 axis plays an essential role in curcumenol-induced ferroptotic cell death. Mechanistically, we showed that lncRNA H19 functioned as a competing endogenous RNA to bind to miR-19b-3p, thereby enhanced the transcription activity of its endogenous target, ferritin heavy chain 1 (FTH1), a marker of ferroptosis. | ||||
Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [3] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Hepatocellular carcinoma | ICD-11: 2C12 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
SMMC-7721 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0534 | |
Huh-7 cells | Hepatocellular carcinoma | Homo sapiens | CVCL_0336 | ||
Hep 3B2.1-7 cells | Hepatocellular carcinoma | Homo sapiens | CVCL_0326 | ||
Hep-G2 cells | Hepatoblastoma | Homo sapiens | CVCL_0027 | ||
L-02 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6926 | ||
In Vivo Model |
C57BL/6 mice (4- to 6-week-old male) were fed in a pathogen-free vivarium under standard conditions at the animal care facility at Sun Yat-sen University. Hepa 1-6 cells transduced with RBMS1 or GPX4 or circIDE overexpression lentiviral vectors were subcutaneously injected into the right flank of mice in 100 ul of sterile PBS. IVIS images were taken.
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|
||||
Response regulation | RBMS1 overexpression inhibited hepatocellular Carcinoma (HCC) cell growth by attenuating the expression of glutathione peroxidase 4 (GPX4)and further facilitated ferroptosis in vitro and in vivo. More importantly, a novel circIDE (hsa_circ_0000251) was identified to elevate RBMS1 expression via sponging miR-19b-3p in HCC cells. | ||||
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-19b-3p (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. | ||||
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [2] | ||||
Target Regulator | hsa-miR-19b-3p (miRNA) | miRNA | |||
Responsed Drug | Curcumenol | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
NCI-H1299 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0060 | |
NCI-H460 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0459 | ||
HEK-293T cells | Normal | Homo sapiens | CVCL_0063 | ||
CCD-19Lu cells | Normal | Homo sapiens | CVCL_2382 | ||
BEAS-2B cells | Normal | Homo sapiens | CVCL_0168 | ||
In Vivo Model |
A subcutaneous tumor-bearing nude mouse model was established by injecting the flank of BALB/c nude mice with 5 x 106 H460 cells. Ten days later, mice were blindly randomized into four groups and intravenously injected with 200 ul ddH2O containing 0.1% CMC-Na and 1% Tween 80, iron chelators DFO (100 mg/kg/day), curcumenol (200 mg/kg/day), and curcumenol combine DFO. Tumor long diameter, short diameter, and body weight were detected every two days after the first drug treatment. The tumor volume calculation formula: (tumor long diameter x tumor short diameter2)/2. Finally, mice were sacrificed. All tumors were collected for immunohistochemical (IHC) staining.
Click to Show/Hide
|
||||
Response regulation | The natural product curcumenol exerted its antitumor effects on lung cancer by triggering ferroptosis, and the lncRNA H19/miR-19b-3p/FTH1 axis plays an essential role in curcumenol-induced ferroptotic cell death. Mechanistically, we showed that lncRNA H19 functioned as a competing endogenous RNA to bind to miR-19b-3p, thereby enhanced the transcription activity of its endogenous target, ferritin heavy chain 1 (FTH1), a marker of ferroptosis. | ||||
Hepatocellular carcinoma [ICD-11: 2C12]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [3] | ||||
Target Regulator | hsa-miR-19b-3p (miRNA) | miRNA | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
SMMC-7721 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0534 | |
Huh-7 cells | Hepatocellular carcinoma | Homo sapiens | CVCL_0336 | ||
Hep 3B2.1-7 cells | Hepatocellular carcinoma | Homo sapiens | CVCL_0326 | ||
Hep-G2 cells | Hepatoblastoma | Homo sapiens | CVCL_0027 | ||
L-02 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6926 | ||
In Vivo Model |
C57BL/6 mice (4- to 6-week-old male) were fed in a pathogen-free vivarium under standard conditions at the animal care facility at Sun Yat-sen University. Hepa 1-6 cells transduced with RBMS1 or GPX4 or circIDE overexpression lentiviral vectors were subcutaneously injected into the right flank of mice in 100 ul of sterile PBS. IVIS images were taken.
Click to Show/Hide
|
||||
Response regulation | RBMS1 overexpression inhibited hepatocellular Carcinoma (HCC) cell growth by attenuating the expression of glutathione peroxidase 4 (GPX4)and further facilitated ferroptosis in vitro and in vivo. More importantly, a novel circIDE (hsa_circ_0000251) was identified to elevate RBMS1 expression via sponging miR-19b-3p in HCC cells. | ||||
Health [ICD-11: N.A.]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [4] | |||
Target Regulator | hsa-miR-19b-3p (miRNA) | miRNA | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
Cell proliferation | ||||
In Vitro Model |
HUVECs (Human umbilical vein endothelial cells) | |||
Response regulation | The upregulated expression of individual miRNAs, miR-17, miR-18a, miR-19a, miR-20a, miR-19b and miR-92 were determined by qRT-PCR. This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis. | |||
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. | ||||
Curcumenol
[Investigative]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [2] | ||||
Drug for Ferroptosis | Inducer | ||||
Response Target | Ferritin heavy chain (FTH1) | Suppressor; Marker | |||
Responsed Disease | Lung cancer | ICD-11: 2C25 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
NCI-H1299 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0060 | |
NCI-H460 cells | Lung large cell carcinoma | Homo sapiens | CVCL_0459 | ||
HEK-293T cells | Normal | Homo sapiens | CVCL_0063 | ||
CCD-19Lu cells | Normal | Homo sapiens | CVCL_2382 | ||
BEAS-2B cells | Normal | Homo sapiens | CVCL_0168 | ||
In Vivo Model |
A subcutaneous tumor-bearing nude mouse model was established by injecting the flank of BALB/c nude mice with 5 x 106 H460 cells. Ten days later, mice were blindly randomized into four groups and intravenously injected with 200 ul ddH2O containing 0.1% CMC-Na and 1% Tween 80, iron chelators DFO (100 mg/kg/day), curcumenol (200 mg/kg/day), and curcumenol combine DFO. Tumor long diameter, short diameter, and body weight were detected every two days after the first drug treatment. The tumor volume calculation formula: (tumor long diameter x tumor short diameter2)/2. Finally, mice were sacrificed. All tumors were collected for immunohistochemical (IHC) staining.
Click to Show/Hide
|
||||
Response regulation | The natural product curcumenol exerted its antitumor effects on lung cancer by triggering ferroptosis, and the lncRNA H19/miR-19b-3p/FTH1 axis plays an essential role in curcumenol-induced ferroptotic cell death. Mechanistically, we showed that lncRNA H19 functioned as a competing endogenous RNA to bind to miR-19b-3p, thereby enhanced the transcription activity of its endogenous target, ferritin heavy chain 1 (FTH1), a marker of ferroptosis. | ||||
References