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Silencing of PTPN18 Induced Ferroptosis in Endometrial Cancer Cells Through p-P38-Mediated GPX4/xCT Down-Regulation
Haibo Wang1, Siyuan Peng1, Junhong Cai2
1Department of Gynaecology and Obstetrics, Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University, Haikou, 570311, People's Republic of China.
Background:
Endometrial cancer (EC) is the fourth most common neoplasm and the eighth leading cause of cancer death in females worldwide. PTPN18 is a member of the protein tyrosine phosphatases (PTP) family, which is associated with the occurrence and progression of various human cancers. PTPN18 was up-regulated in endometrial cancer tissues and high level of PTPN18 promoted proliferation and metastasis of EC cells.
Methods:
The expression of PTPN18, GPX4 and xCT in endometrial cancer tissues and KLE cells was detected by immunohistochemistry and Western blot, respectively. Lentiviral transfection were used to silence PTPN18 level in KLE cells. The Ros level in KLE cells was examined by ELISA assay.
Results:
In the present study, we found that silencing of PTPN18 induced ferroptosis in KLE endometrial cancer cells. PTPN18 knockdown increased intracellular ROS level and down-regulated GPX4 and xCT expression. Besides, silencing of PTPN18 also induced the expression of p-p38.
Conclusion:
We concluded that silencing of PTPN18 might induce ferroptosis by targeting the p-p38/GPX4/xCT axis. The results provide critical insight into the application of PTPN18 knockdown in EC intervention.
Insights
Silencing PTPN18 in endometrial cancer cells induces ferroptosis. This process involves increased reactive oxygen species (ROS) and altered expression of GPX4 and xCT, offering potential therapeutic strategies for EC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Endometrial cancer (EC) is a significant global health concern for women.
- The protein tyrosine phosphatase 18 (PTPN18) is implicated in various cancers.
- Elevated PTPN18 expression correlates with EC progression and metastasis.
Purpose of the Study:
- To investigate the role of PTPN18 in endometrial cancer.
- To explore the potential of PTPN18 modulation in EC treatment.
Main Methods:
- Immunohistochemistry and Western blot to assess PTPN18, GPX4, and xCT expression.
- Lentiviral transfection to silence PTPN18 in KLE cells.
- ELISA assay to measure intracellular reactive oxygen species (ROS) levels.
Main Results:
- PTPN18 knockdown induced ferroptosis in KLE endometrial cancer cells.
- Silencing PTPN18 increased intracellular ROS and decreased GPX4 and xCT expression.
- PTPN18 knockdown also led to increased p-p38 expression.
Conclusions:
- PTPN18 silencing may induce ferroptosis via the p-38/GPX4/xCT pathway.
- Targeting PTPN18 presents a potential therapeutic avenue for endometrial cancer intervention.
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