Identification of PSMD2 as a promising biomarker for pancreatic cancer patients based on comprehensive bioinformatics and in vitro studies
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Proteasome 26S subunit, non-ATPases (PSMDs) are upregulated in pancreatic cancer. PSMD2 drives tumor growth by activating the AKT/mTOR pathway, suggesting it may predict response to AKT inhibitors.
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- Pancreatic cancer has limited treatment options and a poor prognosis.
- Dysregulation of proteasome 26S subunit, non-ATPases (PSMDs) is implicated in various cancers.
- The role of PSMDs in pancreatic cancer remains poorly understood.
Purpose Of The Study
- To explore the therapeutic potential of PSMDs in pancreatic cancer.
- To investigate the prognostic value of PSMDs in pancreatic cancer.
- To elucidate the functional role of PSMD2 and PSMD14 in pancreatic cancer.
Main Methods
- TCGA database analysis of PSMD expression in pancreatic cancer.
- Prognostic value assessment using Cox regression and Kaplan-Meier analyses.
- Functional studies including gene knockdown/overexpression and pathway analysis (AKT/mTOR).
Main Results
- Most PSMDs, notably PSMD2 and PSMD14, were upregulated in pancreatic cancer tissues and associated with worse prognosis.
- PSMD2 overexpression promoted pancreatic cancer cell growth, apoptosis resistance, and gemcitabine resistance by activating the AKT/mTOR pathway.
- PSMD2 expression correlated with immune checkpoint genes but not immune cell infiltration.
Conclusions
- PSMD2 acts as a tumor-promoting protein in pancreatic cancer via AKT/mTOR pathway activation.
- PSMD2 overexpression is a potential biomarker for predicting response to AKT inhibitor therapy in pancreatic cancer patients.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.