EPPK1 (Epiplakin 1)

Notably, YAP overexpression rescued the inhibitory effects of EPPK1 knockdown on OC cell proliferation, migration, invasion, and immune evasion in vitro. The results indicate that EPPK1 promotes immune evasion and distant metastasis in OC by stabilizing YAP RNA.

In addition, interrogation of the Drug-Gene Interaction Database highlighted putative therapeutic targets such as CDK13, MUC16, and MUC17. While preliminary, these findings establish the first comprehensive mutational blueprint of HNLEC, providing novel insights into its pathogenesis, potential prognostic determinants, and therapeutic vulnerabilities, and laying a foundation for future translational and clinical research.

Interestingly, the personalized-treatment targetable alterations, such as microsatellite instability and mismatch repair or homologous recombination deficiencies did not differ between the primary tumors and paired metastases or between the metastases from different secondary sites and had no prognostic value. The results suggest a potential prognostic role of KRAS mutations, mutation load, and CNVs in PDAC patients after metastasectomy and encourage further molecular profiling for personalized treatment of PDAC patients with different metastasis localization.

In addition, we identified specific metabolic pathways involving key metabolites that potentially mediate microbial interactions in CRC. These findings provide new insights into the interplay between the gut microbiome and the mutation landscape of colorectal cancer, thereby informing the clonal evolution of CRC and new strategies for precision medicine.

The preoperative TSUVmax/LSUVmax is a potential predictor of tumor recurrence in patients with HCC following LTx. Its use improves candidate selection and post-LTx management.

Our study highlights the potential significance of epiplakin in colorectal cancer. Decreased epiplakin expression is associated with colon malignancy progression, suggesting its role as a potential marker.

These results revealed that the down-regulation of plakins and the consequential centrosome mispositioning are key signatures of disorganised cytoskeleton networks, inter-cellular junction weakening, shape deregulation and the loss of polarity in breast cancer cells. These metrics could further be used as a new readouts for early phases of tumoral development.

Furthermore, we found mutant MUC16 as an independent protective factor for the prognosis of HCC patients after curative hepatectomy. In conclusion, this study connects genetic abnormalities to clinical practice and potentially identifies individuals with poor prognoses who may benefit from targeted treatment or immunotherapy.

It can identify a subgroup of patients at high risk of recurrence. A more aggressive treatment approach is recommended for these patients.

Our data suggest that EPPK1 is linked to smoking, epithelial to mesenchymal transition, and the regulation of cancer progression, indicating its potential as a therapeutic target for LUAD.

In addition, METTL3 deficiency reduced EPPK1 expression to inactivate the PI3K/AKT pathway. Our results revealed that METTL3 deficiency regulated the m6A modification of EPPK1 to inhibit the PI3K/AKT pathway, thereby restraining the progression of esophageal cancer.

From perspective of SASP, we found detrimental and beneficial tumor subtypes which were closely associated with BCR-free survival for PCa patients, which might be important for the furture research in the field of PCa.