p53 inhibits OTUD5 transcription to promote GPX4 degradation and induce ferroptosis in gastric cancer Article Swipe
Junjing Zhang
,
Tongguan Tian
,
Xinxing Li
,
Kai Xu
,
Yao Lu
,
Xia Li
,
Xinyu Zhao
,
Ziyi Cui
,
Zhenxiang Wang
,
Yuefan Zhou
,
Yixin Xu
,
Hongchen Li
,
Yan Zhang
,
Yu Du
,
Lei Lv
,
Yanping Xu
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1002/ctm2.70271
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1002/ctm2.70271
Background Gastric cancer is one of the most prevalent malignant tumors within the digestive system, and ferroptosis playing a crucial role in its progression. Glutathione peroxidase 4 (GPX4), a key negative regulator of ferroptosis, is highly expressed in gastric cancer and contributes to tumor growth. Targeting the regulation of GPX4 has emerged as a promising approach to induce ferroptosis and develop effective therapy for gastric cancer. Methods To confirm that OTUD5 is a deubiquitinase of GPX4 and regulates ferroptosis, we performed Western blotting, Co‐IP, immunofluorescence, quantitative real‐time PCR, Ub assay and flow cytometry experiments. To explore the physiological function of OUTD5, we knocked out the Otud5 gene in the mouse gastric cancer cell line (MFC) using CRISPR‐Cas9 and eatablished the subcutaneous tumour model. Immunohistochemistry (IHC) analysis was used to inveatigate the pathological correlation in human gastric cancer. Results We report that ovarian tumor domain‐containing 5 (OTUD5) interacts with, deubiquitylates and stabilizes GPX4. OTUD5 depletion destabilizes GPX4, promotes lipid peroxidation and sensitizes gastric cancer cells to ferroptosis. Moreover, the p53 activator nutlin‐3a suppresses OTUD5 transcription, leading to GPX4 degradation and ferroptosis of gastric cancer cells. Notably, only wild‐type p53 has the capacity to inhibit OTUD5 transcription, while p53 mutations or deficiencies correlate with increased OTUD5 expression, promoting gastric cancer progression. Additionally, OTUD5 silencing and nutlin‐3a‐induced GPX4 degradation enhances the sensitivity of gastric cancer cells to ferroptosis in vivo. Subsequently, the p53/OTUD5/GPX4 axis is confirmed in clinical gastric cancer samples. Conclusion Collectively, these findings elucidate a mechanism whereby p53 inactivation upregulates OTUD5 transcription to deubiquitylate and stablize GPX4, resulting in ferroptosis inhibition and gastric cancer progression. This discovery highlights the potential therapeutic value of targeting OTUD5 to promote ferroptosis in p53‐inactivated gastric cancer. Key points OTUD5 mediates GPX4 deubiquitination to regulate its stability. Deletion of OTUD5 promotes ferroptosis and inhibits tumor growth. Wild type p53 inhibits OTUD5 transcription, thereby promoting GPX4 degradation and inhibiting the development of gastric cancer. OTUD5, GPX4 expression and p53 activity are highly correlated and correlates with clinical progression in STAD.
Related Topics
Concepts
GPX4
Cancer research
Cancer
Cancer cell
Apoptosis
Biology
Glutathione
Glutathione peroxidase
Biochemistry
Enzyme
Genetics
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/ctm2.70271
- https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/ctm2.70271
- OA Status
- gold
- Cited By
- 7
- References
- 44
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4408377190
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4408377190Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1002/ctm2.70271Digital Object Identifier
- Title
-
p53 inhibits OTUD5 transcription to promote GPX4 degradation and induce ferroptosis in gastric cancerWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-03-01Full publication date if available
- Authors
-
Junjing Zhang, Tongguan Tian, Xinxing Li, Kai Xu, Yao Lu, Xia Li, Xinyu Zhao, Ziyi Cui, Zhenxiang Wang, Yuefan Zhou, Yixin Xu, Hongchen Li, Yan Zhang, Yu Du, Lei Lv, Yanping XuList of authors in order
- Landing page
-
https://doi.org/10.1002/ctm2.70271Publisher landing page
- PDF URL
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/ctm2.70271Direct link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/ctm2.70271Direct OA link when available
- Concepts
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GPX4, Cancer research, Cancer, Cancer cell, Apoptosis, Biology, Glutathione, Glutathione peroxidase, Biochemistry, Enzyme, GeneticsTop concepts (fields/topics) attached by OpenAlex
- Cited by
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7Total citation count in OpenAlex
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2025: 7Per-year citation counts (last 5 years)
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44Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| citation_normalized_percentile.value | 0.99317094 |
| citation_normalized_percentile.is_in_top_1_percent | True |
| citation_normalized_percentile.is_in_top_10_percent | True |