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PSMD12 promotes hepatocellular carcinoma progression by stabilizing CDK1
Xingyu Peng1,2, Zitao Liu1,2, Chen Luo3
1Department of General Surgery, The 2nd Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Frontiers in Immunology
|June 19, 2025
Summary
Proteasome 26S subunit non-ATPase 12 (PSMD12) is upregulated in hepatocellular carcinoma (HCC), promoting tumor growth and poor prognosis. Targeting PSMD12 may offer a new therapeutic strategy for HCC patients.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- The proteasome system maintains protein homeostasis.
- The specific role of Proteasome 26S subunit non-ATPase 12 (PSMD12) in hepatocellular carcinoma (HCC) is not well understood.
- Understanding PSMD12's function in HCC is crucial for identifying new therapeutic targets.
Purpose of the Study:
- To investigate the role of PSMD12 in hepatocellular carcinoma (HCC).
- To determine if PSMD12 can serve as a prognostic biomarker and therapeutic target for HCC.
Main Methods:
- Bioinformatics analysis
- Immunohistochemistry
- Western blotting
- qRT-PCR
- Functional assays (cell proliferation, migration, cell cycle analysis)
- Co-immunoprecipitation to study protein interactions.
Main Results:
- PSMD12 was significantly upregulated in HCC tissues compared to normal liver tissues.
- High PSMD12 expression correlated with poor patient prognosis.
- PSMD12 knockdown inhibited HCC cell proliferation and migration, causing G2/M cell cycle arrest.
- PSMD12 overexpression enhanced HCC cell malignant behaviors.
- PSMD12 interacts with CDK1, inhibiting its degradation and promoting cell cycle progression.
Conclusions:
- PSMD12 plays a critical role in promoting HCC progression.
- PSMD12 functions by stabilizing CDK1, thereby accelerating cell cycle progression.
- PSMD12 is a potential prognostic biomarker and therapeutic target for hepatocellular carcinoma.
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