TRIP13 (Thyroid Hormone Receptor Interactor 13)

TRIP13 is identified as a potential oncogenic gene in ovarian cancer. Its high expression and association with advanced disease highlight its value as a biomarker and potential therapeutic target.

Functional enrichment analyses indicated that apigenin-regulated genes are involved in multiple cancer-related pathways across cytoplasmic and nuclear compartments. Overall, these results suggest that apigenin suppresses ESCC progression via coordinated miRNA-mRNA regulation, highlighting its potential as a therapeutic agent.

P2, N=50, Recruiting, Universiteit Antwerpen

P2, N=50, Recruiting, Universiteit Antwerpen | Not yet recruiting --> Recruiting

Mgenes modulate ULMS's TIME, offering immunotherapeutic targets. This study advances ULMS molecular/immune understanding for translational research.

P2, N=50, Not yet recruiting, Universiteit Antwerpen

Using this cell line, we showed that splicing to the HPV16 E2 3'-splice site SA2709 could be perturbed by over expression of SR-proteins or by incubation with a pan-Akt kinase inhibitor. These proteins and substances shifted splicing from E2 splice site SA2709 to the upstream HPV16 3'-splice site SA2582 and enhanced nLuc production, thereby demonstrating the utility of the pE1nLuc cell line as a bioassay for HPV16 E2 mRNA splicing.

We also established a subcutaneous transplantation tumor model in NB NOD/scid mice, and sh-LINC01296 or sh-TRIP13 inhibited tumor growth in mice, and the tumor growth in the sh-LINC01296 + OE-TRIP13 group and the sh-TRIP13 + OE-LINC01296 group was between the NC group and the sh-LINC01296 or sh-TRIP13 group. These results suggest that LINC01296 may play a role as an oncogene in the development of tumorigenesis in NB by mediating TRIP13, and provide a marker for the prognosis of NB.

Ultimately, understanding the genetic regulation of DSB repair pathways can provide critical insights into genome stability maintenance and reveal new therapeutic opportunities in cancer. Future work should focus on pathway crosstalk, phase-specific regulation, and integrating repair modulation into personalized medicine.

The development of ccRCC is significantly influenced by MRGs, particularly TRIP13. This study can assist in offering ccRCC patients individualized treatment options.

These findings uncover a previously unrecognized role of TRIP13 in regulating mitochondrial integrity under proteotoxic stress, thereby contributing to BTZ resistance. Targeting TRIP13 may represent a novel therapeutic approach to improve outcomes in MM patients.

Interestingly, TRIP13 reciprocally regulates the stability of the CSE1L protein, indicating a bidirectional regulatory loop. The CSE1L-TRIP13 axis provides a robust theoretical foundation to develop targeted therapeutic strategies, offering novel insights into the clinical treatment of GC patients.