Ferroptosis-centered Drug Response Information
General Information of the Drug (ID: ferrodrug0423)
Name |
Antagomir
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Drug Type |
Small molecule
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Full List of Ferroptosis Target Related to This Drug
Neutral amino acid transporter B(0) (SLC1A5)
In total 1 item(s) under this Target | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Melanoma | ICD-11: 2C30 | |||
Responsed Regulator | hsa-mir-137 (Precursor RNA) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Glutamate metabolism | hsa00250 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | A-375 cells | Amelanotic melanoma | Homo sapiens | CVCL_0132 | |
G-361 cells | Melanoma | Homo sapiens | CVCL_1220 | ||
In Vivo Model |
To generate murine subcutaneous tumors, melanoma cells (5 x 106 cells per mouse) were injected subcutaneously into the right posterior flanks of 7-week-old immunodeficient nude mice. When tumors reached a volume of approximately 50 mm3, mice were randomly allocated into groups and treated with erastin for 20 days. The erastin was dissolved in 5% dimethylsulfoxide (DMSO) + corn oil (C8267, Sigma).
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Response regulation | MiR-137 negatively regulates ferroptosis by directly targeting glutamine transporter SLC1A5 in melanoma cells. Ectopic expression of miR-137 suppressed SLC1A5, resulting in decreased glutamine uptake and malondialdehyde (MDA) accumulation. Meanwhile, antagomir-mediated inactivation of endogenous miR-137 increased the sensitivity of melanoma cells to erastin- and RSL3-induced ferroptosis. | ||||