Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10157)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
ETV4
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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Cystine/glutamate transporter (SLC7A11) [Driver; Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Thyroid cancer | ICD-11: 2D10 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell cycle | |||||
In Vitro Model |
TPC-1 cells | Thyroid gland papillary carcinoma | Homo sapiens | CVCL_6298 | |
IHH-4 cells | Thyroid gland papillary carcinoma | Homo sapiens | CVCL_2960 | ||
Nthy-ori3-1 cells | Normal | Homo sapiens | CVCL_2659 | ||
In Vivo Model |
Six-week-old BALB/c female nude mice (HFK Bioscience, Beijing, China) were used to perform experimentsin vivo. One hundred forty-four mice were randomly divided into four groups (36 mice in each group). TPC-1 cells were stably transfected with NC shRNA or ETV4-shRNA, and GLAG-66 cells were stably transfected with ETV4-OE or Vector. 5 x 106 cells were injected subcutaneously into the right armpit in mice. After 7 days, the diameter of tumors was measured every 3 days to calculate the tumor volume.
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Response regulation | The downregulation of ETV4 repressed the tumor development through the low expression of SLC7A11, and the ETV4 overexpression obtained the contrary effects. Overall, knockdown of ETV4 suppressed the papillary thyroid cancer progression by promoting ferroptosis upon SLC7A11 downregulation. | ||||
Thyroid cancer [ICD-11: 2D10]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | ETS translocation variant 4 (ETV4) | Protein coding | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell cycle | |||||
In Vitro Model |
TPC-1 cells | Thyroid gland papillary carcinoma | Homo sapiens | CVCL_6298 | |
IHH-4 cells | Thyroid gland papillary carcinoma | Homo sapiens | CVCL_2960 | ||
Nthy-ori3-1 cells | Normal | Homo sapiens | CVCL_2659 | ||
In Vivo Model |
Six-week-old BALB/c female nude mice (HFK Bioscience, Beijing, China) were used to perform experimentsin vivo. One hundred forty-four mice were randomly divided into four groups (36 mice in each group). TPC-1 cells were stably transfected with NC shRNA or ETV4-shRNA, and GLAG-66 cells were stably transfected with ETV4-OE or Vector. 5 x 106 cells were injected subcutaneously into the right armpit in mice. After 7 days, the diameter of tumors was measured every 3 days to calculate the tumor volume.
Click to Show/Hide
|
||||
Response regulation | The downregulation of ETV4 repressed the tumor development through the low expression of SLC7A11, and the ETV4 overexpression obtained the contrary effects. Overall, knockdown of ETV4 suppressed the papillary thyroid cancer progression by promoting ferroptosis upon SLC7A11 downregulation. | ||||