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Updated: Aug 14, 2025
A Murine Orthotopic Bladder Tumor Model and Tumor Detection System
Published on: January 12, 2017
Depletion of PSMD14 suppresses bladder cancer proliferation by regulating GPX4
Changxin Jia1, Xin Zhang1, Tingting Qu2
1Department of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Objective:
The aim of this study was to investigate the role of deubiquitinase (DUB) 26S proteasome non-ATPase regulatory subunit 14 (PSMD14) in patients with bladder cancer.
Methods:
From 2016 to 2018, 181 patients diagnosed with primary bladder cancer at the Affiliated Hospital of Qingdao University were recruited. The expression of PSMD14 in bladder cancer tissues was tested by immunochemistry. The association between PSMD14 expression and clinical and pathological data and outcomes of bladder cancer patients was determined. Overexpression and knockdown cells were constructed to evaluate the effects of PSMD14 on proliferation of bladder cancer cells.
Results:
Our results showed that PSMD14 was significantly overexpressed in bladder cancer tissues compared to adjacent non-tumor tissues (76.24% vs 23.76%, P = 0.02). The expression of PSMD14 was significantly higher in patients with larger tumor diameters (85.14% vs 70.09%, P = 0.019) and patients with a family history of cancer (92.16% vs 70.00%, P = 0.002). Patients with high expression of PSMD14 had poor disease-free survival (DFS) (HR = 2.89, 95% CI [1.247-6.711], P = 0.013). Gain and loss of function experiments demonstrated that PSMD14 deficiency inhibited bladder cancer cell proliferation. Additionally, depletion of PSMD14 suppressed bladder cancer cell growth via down-regulation of GPX4, and the promotion of PSMD14-induced cell growth was observably reversed by the GPX4 inhibitor RSL3.
Conclusion:
We determined that PSMD14 is highly expressed in bladder cancer tissues, and that PSMD14 expression correlated with poor disease-free survival. Depletion of PSMD14 could inhibit the proliferation of bladder cancer cells through the downregulation of GPX4. Therefore, PSMD14 may be an effective target for the treatment of bladder cancer.
Insights
The deubiquitinase PSMD14 is overexpressed in bladder cancer, correlating with poor survival. Inhibiting PSMD14 suppressed cancer cell growth by downregulating GPX4, suggesting PSMD14 as a potential bladder cancer treatment target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Bladder cancer remains a significant health concern with limited targeted therapies.
- Deubiquitinase enzymes play crucial roles in cellular processes, and their dysregulation is implicated in various cancers.
Purpose of the Study:
- To investigate the role of deubiquitinase 26S proteasome non-ATPase regulatory subunit 14 (PSMD14) in bladder cancer.
- To determine the correlation between PSMD14 expression and clinical outcomes in bladder cancer patients.
Main Methods:
- Immunohistochemistry was used to assess PSMD14 expression in 181 bladder cancer tissues and adjacent non-tumor tissues.
- Correlation analysis was performed between PSMD14 expression and clinical/pathological data.
- In vitro experiments (overexpression and knockdown) evaluated the impact of PSMD14 on bladder cancer cell proliferation and the role of GPX4.
Main Results:
- PSMD14 was significantly overexpressed in bladder cancer tissues (76.24%) compared to non-tumor tissues (23.76%).
- High PSMD14 expression correlated with larger tumor size and a family history of cancer.
- Elevated PSMD14 levels were associated with poor disease-free survival (DFS).
- PSMD14 depletion inhibited bladder cancer cell proliferation by downregulating GPX4, an effect reversed by a GPX4 inhibitor.
Conclusions:
- PSMD14 is highly expressed in bladder cancer and linked to unfavorable prognosis.
- PSMD14 inhibition suppresses bladder cancer cell proliferation via GPX4 downregulation.
- PSMD14 represents a potential therapeutic target for bladder cancer treatment.
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