General Information of the Ferroptosis Regulator (ID: REG20027)
Regulator Name hsa-miR-144-3p (miRNA)
Synonyms
hsa-miR-144-3p
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Gene Name hsa-miR-144-3p
Regulator Type miRNA
MiRBase ID MIMAT0000436
Sequence
UACAGUAUAGAUGAUGUACU

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Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-144-3p 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 [2]
Target for Ferroptosis Driver
Responsed Disease Osteosarcoma ICD-11: 2B51
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell migration
Cell invasion
In Vitro Model
143B cells Osteosarcoma Homo sapiens CVCL_2270
SW1353 cells Bone chondrosarcoma Homo sapiens CVCL_0543
MG-63 cells Osteosarcoma Homo sapiens CVCL_0426
SAOS-2 cells Osteosarcoma Homo sapiens CVCL_0548
U2OS cells Osteosarcoma Homo sapiens CVCL_0042
HOB (Human normal osteoblastic cells)
In Vivo Model
The OS model of nude mice was constructed using the CDTX model. After transfection, the h143B cells were prepared into a single-cell suspension and subcutaneously injected into the left proximal tibia of 36 (3 mice per group) 4-weeks-old nude mice (1 x 107 cells per mouse).

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Response regulation MiR-144-3p can induce the occurrence of ferroptosis by negatively regulating the expression of ZEB1, thereby inhibiting the proliferation, migration, and invasion of osteosarcoma (OS) cells. The overexpression of ZEB1 caused the lower expression level of ACSL4 and higher expression level of xCT and GPX4.
Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [2]
Target for Ferroptosis Suppressor
Responsed Disease Osteosarcoma ICD-11: 2B51
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell migration
Cell invasion
In Vitro Model
143B cells Osteosarcoma Homo sapiens CVCL_2270
SW1353 cells Bone chondrosarcoma Homo sapiens CVCL_0543
MG-63 cells Osteosarcoma Homo sapiens CVCL_0426
SAOS-2 cells Osteosarcoma Homo sapiens CVCL_0548
U2OS cells Osteosarcoma Homo sapiens CVCL_0042
HOB (Human normal osteoblastic cells)
In Vivo Model
The OS model of nude mice was constructed using the CDTX model. After transfection, the h143B cells were prepared into a single-cell suspension and subcutaneously injected into the left proximal tibia of 36 (3 mice per group) 4-weeks-old nude mice (1 x 107 cells per mouse).

    Click to Show/Hide
Response regulation MiR-144-3p can induce the occurrence of ferroptosis by negatively regulating the expression of ZEB1, thereby inhibiting the proliferation, migration, and invasion of osteosarcoma (OS) cells. The overexpression of ZEB1 caused the lower expression level of ACSL4 and higher expression level of xCT and GPX4.
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-144-3p (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.
Osteosarcoma [ICD-11: 2B51]
In total 2 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator hsa-miR-144-3p (miRNA) miRNA
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell migration
Cell invasion
In Vitro Model
143B cells Osteosarcoma Homo sapiens CVCL_2270
SW1353 cells Bone chondrosarcoma Homo sapiens CVCL_0543
MG-63 cells Osteosarcoma Homo sapiens CVCL_0426
SAOS-2 cells Osteosarcoma Homo sapiens CVCL_0548
U2OS cells Osteosarcoma Homo sapiens CVCL_0042
HOB (Human normal osteoblastic cells)
In Vivo Model
The OS model of nude mice was constructed using the CDTX model. After transfection, the h143B cells were prepared into a single-cell suspension and subcutaneously injected into the left proximal tibia of 36 (3 mice per group) 4-weeks-old nude mice (1 x 107 cells per mouse).

    Click to Show/Hide
Response regulation MiR-144-3p can induce the occurrence of ferroptosis by negatively regulating the expression of ZEB1, thereby inhibiting the proliferation, migration, and invasion of osteosarcoma (OS) cells. The overexpression of ZEB1 caused the lower expression level of ACSL4 and higher expression level of xCT and GPX4.
Experiment 2 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator hsa-miR-144-3p (miRNA) miRNA
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell migration
Cell invasion
In Vitro Model
143B cells Osteosarcoma Homo sapiens CVCL_2270
SW1353 cells Bone chondrosarcoma Homo sapiens CVCL_0543
MG-63 cells Osteosarcoma Homo sapiens CVCL_0426
SAOS-2 cells Osteosarcoma Homo sapiens CVCL_0548
U2OS cells Osteosarcoma Homo sapiens CVCL_0042
HOB (Human normal osteoblastic cells)
In Vivo Model
The OS model of nude mice was constructed using the CDTX model. After transfection, the h143B cells were prepared into a single-cell suspension and subcutaneously injected into the left proximal tibia of 36 (3 mice per group) 4-weeks-old nude mice (1 x 107 cells per mouse).

    Click to Show/Hide
Response regulation MiR-144-3p can induce the occurrence of ferroptosis by negatively regulating the expression of ZEB1, thereby inhibiting the proliferation, migration, and invasion of osteosarcoma (OS) cells. The overexpression of ZEB1 caused the lower expression level of ACSL4 and higher expression level of xCT and GPX4.
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
Ref 1 Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis. Anim Cells Syst (Seoul). 2018 Aug 30;22(5):334-340. doi: 10.1080/19768354.2018.1512521. eCollection 2018.
Ref 2 Exosome-mediated miR-144-3p promotes ferroptosis to inhibit osteosarcoma proliferation, migration, and invasion through regulating ZEB1. Mol Cancer. 2023 Jul 17;22(1):113. doi: 10.1186/s12943-023-01804-z.