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GID2 Interacts With CDKN3 and Regulates Pancreatic Cancer Growth and Apoptosis
Xin Deng1, Jia Ma2, Wenyang Zhou3
1Pancreatic Endocrinology Ward, Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
Laboratory Investigation; a Journal of Technical Methods and Pathology
|February 24, 2023
Summary
Glucose-induced degradation-deficient 2 (GID2) promotes pancreatic cancer (PC) progression by stabilizing the cell cycle regulator CDKN3. Targeting the GID2/CDKN3 pathway may offer new therapeutic strategies for pancreatic cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Dysregulation of protein expression via ubiquitination pathways is implicated in various diseases, including cancer.
- The glucose-induced degradation-deficient (GID) complex subunit GID2, an E3 ubiquitin ligase, is investigated for its role in pancreatic cancer (PC).
Purpose of the Study:
- To investigate the functional role and underlying mechanism of GID2 in pancreatic cancer progression.
- To identify potential therapeutic targets within the GID2 regulatory network in PC.
Main Methods:
- Integrated bioinformatics analysis of Gene Expression Profiling Interactive Analysis (GEPIA) datasets.
- In vitro and in vivo functional assays including GID2 knockdown.
- Protein-protein interaction network construction using GeneMANIA.
- Analysis of GID2 and CDKN3 ubiquitination levels.
Main Results:
- GID2 was found to be upregulated in PC tissues and associated with advanced tumor stage and poor survival.
- GID2 overexpression promoted PC cell growth in vitro and tumor growth in vivo, while knockdown attenuated these effects.
- GID2 was identified to stabilize Cyclin-dependent kinase inhibitor 3 (CDKN3) by inhibiting its ubiquitination, thereby promoting PC progression.
Conclusions:
- GID2 promotes pancreatic cancer progression by enhancing the stability of the cell cycle regulator CDKN3.
- The GID2/CDKN3 axis represents a potential therapeutic target for pancreatic cancer treatment.
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