Ferroptosis-centered Disease Response Information
General Information of the Disease (ID: DIS00039)
| Name |
Uterine serous carcinoma
|
||||
|---|---|---|---|---|---|
| ICD |
ICD-11: 2C72
|
||||
Full List of Target(s) of This Ferroptosis-centered Disease
Cystine/glutamate transporter (SLC7A11)
| 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 | Uterine serous carcinoma [ICD-11: 2C72] | ||||
| Responsed Drug | Sulfasalazine | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
| In Vitro Model | hUPSCs (Human uterine serous papillary carcinoma-1 cells) | ||||
| Abcam HeLa ERGIC2 KO cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_B1RG | ||
| SK-OV-3 cells | Ovarian serous cystadenocarcinoma | Homo sapiens | CVCL_0532 | ||
| In Vivo Model |
The mean weight of the mice at the start was 19.4 ± 0.87 g. To generate the subcutaneous xenograft model, USPC1 (5 x 106 cells) or PTX1 (5 x 106 cells) were suspended in 200 ul of PBS following determination of cellular viability and injected into the subcutaneous tissue of 6-week-old female Crj:SHO-PrkdcscidHrhr hairless SCID mice (n = 2) (Charles River Laboratories Inc.). Tumor formation was visually confirmed in mice inoculated with USPC1 cells, but not in those inoculated with PTX1 cells, thus the animal study was performed using USPC1 cells. The recipient mice were monitored for general health status and presence of subcutaneous tumors once a week.
Click to Show/Hide
|
||||
| Response regulation | The effect of the xCT (SLC7A11) inhibitor, sulfasalazine on cytotoxicity was stronger in paclitaxel-resistant uterine serous carcinoma (USC) cells compared with that in paclitaxel-sensitive USC cells. Furthermore, the synthetic lethal interaction between the accumulation of ROS and the activation of the Ras effector, JNK, induced cell-proliferation inhibition and ferroptotic cell death in paclitaxel-resistant USC cells. | ||||