Ferroptosis-centered Disease Response Information
General Information of the Disease (ID: DIS00024)
Name |
Oral squamous cell carcinoma
|
||||
---|---|---|---|---|---|
ICD |
ICD-11: 2B6E
|
Full List of Target(s) of This Ferroptosis-centered Disease
Phospholipid hydroperoxide glutathione peroxidase (GPX4)
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Tongue squamous cell carcinoma [ICD-11: 2B6E] | ||||
Responsed Drug | Quisinostat | Investigative | |||
Responsed Regulator | Cellular tumor antigen p53 (TP53) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Apoptosis | hsa04210 | ||||
Necroptosis | hsa04217 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell apoptosis | |||||
Cell pyroptosis | |||||
In Vitro Model | CAL-27 cells | Tongue adenosquamous carcinom | Homo sapiens | CVCL_1107 | |
Tca8113 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6851 | ||
In Vivo Model |
Adult male athymic BALB/c nude mice (20-22 g of 5-week-old mice) were housed in a controlled environment at 23 ± 2 and 40%-70% humidity under a 12 h dark/light cycle with free access to irradiated food and sterile water. A suspension of 6 x 106/100 uL TCA-8113 cells was inoculated subcutaneously into the hind flank region of each nude mouse. The average tumor volume in nude mice reached 100 mm3, and mice were randomly divided into three groups. Quisinostat was formulated in normal saline and administered at 3 and 10 mg/kg/day byintraperitoneal injection. Control mice were given equal volume saline intraperitoneally. The tumor volume and the bodyweight of mice were monitored every three days.
Click to Show/Hide
|
||||
Response regulation | Quisinostat could increase the apoptosis rate in the tumor tissues of nude mice. Up-regulation of the expression of p53 and down-regulated expression of GPX4 in cell lines were observed by immunofluorescent staining, and the expression locations of p53 and GPX4 proteins in TSCC cells were observed. Quisinostat may be a potential drug for the treatment of tongue squamous cell carcinoma. | ||||
Nuclear factor erythroid 2-related factor 2 (NFE2L2)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Marker/Suppressor | |||
Responsed Disease | Oral squamous cell carcinoma [ICD-11: 2B6E.0] | |||
Responsed Drug | Carnosic acid | Investigative | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Cell Process | Cell ferroptosis | |||
Response regulation | The current findings highlight that carnosic acid may re-sensitize cisplatin-resistant cells to cisplatin by inducing ferroptosis, which involves the inactivation of Nrf2/HO-1/xCT pathway. Hence, this research may support a promising therapeutic approach to overcome chemoresistance in Oral squamous cell carcinoma. | |||
Heme oxygenase 1 (HMOX1)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Oral squamous cell carcinoma [ICD-11: 2B6E.0] | |||
Responsed Drug | Carnosic acid | Investigative | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Cell Process | Cell ferroptosis | |||
Response regulation | The current findings highlight that carnosic acid may re-sensitize cisplatin-resistant cells to cisplatin by inducing ferroptosis, which involves the inactivation of Nrf2/HO-1/xCT pathway. Hence, this research may support a promising therapeutic approach to overcome chemoresistance in Oral squamous cell carcinoma. | |||
Cystine/glutamate transporter (SLC7A11)
In total 5 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [3] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Tongue squamous cell carcinoma [ICD-11: 2B6E] | ||||
Responsed Regulator | Histone-lysine N-methyltransferase EZH2 (EZH2) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model | Tca8113 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6851 | |
TSCCA cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_VL15 | ||
CAL-27 cells | Tongue adenosquamous carcinom | Homo sapiens | CVCL_1107 | ||
SCC-9 cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1685 | ||
hTECs (Human tongue epithelial cells) | |||||
Response regulation | EZH2 inhibits the ferroptosis of tongue squamous cell carcinoma cells by inhibiting miR-125b-5p and enhancing SLC7A11. MiR-125b-5p regulates ferroptosis in TSCC cells by targeting SLC7A11. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [4] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Oral squamous cell carcinoma [ICD-11: 2B6E.0] | ||||
Responsed Regulator | hsa-miR-34c-3p (miRNA) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | SCC-25 cells | Squamous carcinoma | Homo sapiens | CVCL_1682 | |
CAL-27 cells | Tongue adenosquamous carcinom | Homo sapiens | CVCL_1107 | ||
HOK cells | Normal | Hexagrammos otakii | CVCL_YE19 | ||
Response regulation | Low expression of miR-34c-3p in oral squamous cell carcinoma, negatively regulating SLC7A11 expression, promoting ferroptosis, and suppressing cell proliferation. | ||||
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target | [3] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Tongue squamous cell carcinoma [ICD-11: 2B6E] | ||||
Responsed Regulator | hsa-miR-125b-5p (miRNA) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model | Tca8113 cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_6851 | |
TSCCA cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_VL15 | ||
CAL-27 cells | Tongue adenosquamous carcinom | Homo sapiens | CVCL_1107 | ||
SCC-9 cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1685 | ||
hTECs (Human tongue epithelial cells) | |||||
Response regulation | EZH2 inhibits the ferroptosis of tongue squamous cell carcinoma cells by inhibiting miR-125b-5p and enhancing SLC7A11. MiR-125b-5p regulates ferroptosis in TSCC cells by targeting SLC7A11. | ||||
Experiment 4 Reporting the Ferroptosis-centered Disease Response by This Target | [5] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Oral squamous cell carcinoma [ICD-11: 2B6E.0] | ||||
Responsed Regulator | hsa-miR-520d-5p (miRNA) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | CAL-27 cells | Tongue adenosquamous carcinom | Homo sapiens | CVCL_1107 | |
SCC-15 cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1681 | ||
In Vivo Model |
The tumorigenicity analysis was conducted in BALB/c nude mice (6-weeks-old, male). The mice were maintained at pathogen-free condition. The 5 x 106 CAL27 cells were treated with control shRNA or circFNDC3B shRNA and subcutaneously injected into the nude mice (N = 5). The mice were sacrificed after 30 days and the tumor volume was calculated using the formula of (length x width2)/2.
Click to Show/Hide
|
||||
Response regulation | CircFNDC3B attenuated ferroptosis of Oral squamous cell carcinoma (OSCC) cells and contributed to OSCC progression by regulating the miR-520d-5p/SLC7A11 axis. CircFNDC3B, miR-520d-5p, and SLC7A11 may serve as potential therapeutic targets of OSCC. | ||||
Experiment 5 Reporting the Ferroptosis-centered Disease Response by This Target | [5] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Oral squamous cell carcinoma [ICD-11: 2B6E.0] | ||||
Responsed Regulator | CircFNDC3B (circRNA) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | CAL-27 cells | Tongue adenosquamous carcinom | Homo sapiens | CVCL_1107 | |
SCC-15 cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1681 | ||
In Vivo Model |
The tumorigenicity analysis was conducted in BALB/c nude mice (6-weeks-old, male). The mice were maintained at pathogen-free condition. The 5 x 106 CAL27 cells were treated with control shRNA or circFNDC3B shRNA and subcutaneously injected into the nude mice (N = 5). The mice were sacrificed after 30 days and the tumor volume was calculated using the formula of (length x width2)/2.
Click to Show/Hide
|
||||
Response regulation | CircFNDC3B attenuated ferroptosis of Oral squamous cell carcinoma (OSCC) cells and contributed to OSCC progression by regulating the miR-520d-5p/SLC7A11 axis. CircFNDC3B, miR-520d-5p, and SLC7A11 may serve as potential therapeutic targets of OSCC. | ||||
References