Recent advances have shed light on the structural basis of gankyrin's molecular interactions, its potential as a diagnostic and prognostic biomarker, and emerging therapeutic strategies. Together, targeting gankyrin represents a promising strategy for precision oncology in GI cancers.
Our findings suggest that increase expression levels of Derlin1 and PSMD10 genes in HeLa cells by the EBV-EBNA1 might induce cancer cell survival and accelerates the development of cervical cancer (CC). However, to establish a conclusive link between EBV-EBNA1 and CC progression, further investigations are warranted.
These findings suggest that Gankyrin plays a crucial role in H. pylori-mediated GC progression by modulating inflammatory and tumor suppressor pathways. Targeting Gankyrin could provide a therapeutic strategy to mitigate the development of GC associated with H. pylori infection.
We discovered a significant correlation between aberrant expression of URGs and prognosis in SARC patients, identifying a prognostic model related to ubiquitination. This model provides a basis for individualized treatment and immunotherapy decisions for SARC patients.
It seems that EBNA1 could strongly upregulate p53-inhibiting genes including HDAC1, MDM2, MDM4, and USP7. Moreover, it appears that the effects of USP7 suppression on p53 at protein/mRNA level depend on the cell nature; however, further research is needed.
Two events-p53 protein overexpression and apoptosis activation-followed the suppression of the USP7 protein and provided evidence for its possible function. The significance of the EBNA1-USP7 interaction in p53 suppression warrants additional investigation and possibly reconsideration.
MALAT1 competitively binds to miR-188-5p to up-regulate mRNA translation and protein expression of PSMD10, thereby facilitating cholangiocarcinoma cell invasion and migration and inhibiting its apoptosis. However, interfering MALAT1-miR-188-5p-PSMD10 axis could inhibit the occurrence and development of cholangiocarcinoma.
STAT3 could occupy the miR-1254 promoter to inhibit transcription, and it could suppressed miR-1254 which targeted PSMD10, promoting proteasome 20S α+β protein stability. This is a prospective target for developing a new colorectal cancer therapy strategy.
Our study, for the first time, shows that PSMD10 is required for the activation of the pro-survival arm via NFκB transcriptional activation to prevent cancer cells from succumbing to TNF-induced cell death. In addition by transcriptional regulation of two major antiapoptotic players RB1 and β-catenin, PSMD10 proves to be a coveted oncoprotein with a key role in tumorigenesis.
Functional assays by targeting SERPINE1 expression revealed that the malignant phenotypes (e.g., proliferation, migration, and invasion abilities) of HNSCC cells were suppressed by the silencing of SERPINE1 expression. Our miRNA-based approach will accelerate our understanding of the molecular pathogenesis of HNSCC.
almost 4 years ago
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HMGA2 (High mobility group AT-hook 2) • SERPINE1 (Serpin Family E Member 1) • PSMD10 (Proteasome 26S Subunit Non-ATPase 10) • MIR30E (MicroRNA 30e)