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Updated: Apr 1, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
KDM3A interacted with p53K372me1 and regulated p53 binding to PUMA in gastric cancer
Wenfeng Li1, Shuangming Lin1, Wenhuan Li2
1The Department of Gastrointestinal and Anus Surgery, The Affiliated Longyan First Hospital of Fujian Medical University, Longyan 364000, Fujian Province, PR China.
Abstract:
Chemoresistance remains a major problem in the treatment of gastric cancer patients, leading to the serious limitation of efficacy of chemotherapeutic regime. However, the underlying mechanism remains largely unknown. In our present study, we for the first time found that knock down of KDM3A can promote apoptosis induced by chemoreagent Cisplatin and Paclitaxel through p53. Mechanistically, through promoting p53 binding to the promoter of PUMA. However, knock down of KDM3A as such doesn't affect p53 level. In addition, KDM3A can interact with p53K372me1 in protein-protein interaction fashion, leading to the inactivation of p53, may eventually leading to chemoresistance of gastric cancer.
Insights
Knocking down KDM3A enhances chemotherapy effectiveness in gastric cancer by promoting p53-mediated apoptosis. This study reveals KDM3A
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Chemoresistance significantly limits gastric cancer treatment efficacy.
- The molecular mechanisms driving chemoresistance are not fully understood.
Purpose of the Study:
- To investigate the role of KDM3A in gastric cancer chemoresistance.
- To elucidate the mechanism by which KDM3A influences chemotherapy response.
Main Methods:
- Utilized knockdown of KDM3A in gastric cancer models.
- Assessed apoptosis induction by chemotherapeutic agents (Cisplatin, Paclitaxel).
- Investigated p53 pathway activation and protein-protein interactions.
Main Results:
- KDM3A knockdown promotes apoptosis induced by Cisplatin and Paclitaxel.
- KDM3A knockdown enhances p53 binding to the PUMA promoter, increasing apoptosis.
- KDM3A interacts with p53K372me1, potentially inactivating p53 and contributing to chemoresistance.
Conclusions:
- KDM3A plays a critical role in gastric cancer chemoresistance.
- Targeting KDM3A may represent a novel therapeutic strategy to overcome chemoresistance.
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