PRKCH (Protein Kinase C Eta)

Finally, we show that an evolutionarily conserved peptide encoded by an upstream open reading frame (uORF) preceding the PKCη coding sequence functions as a PKCη degrader, activating the Hippo pathway and promoting YAP degradation. Together, our findings reveal a PKCη-driven signaling axis that regulates the Hippo-YAP pathway in TNBC metastasis, highlighting the potential therapeutic vulnerability of this aggressive disease.

Wavelet-based individualized brain structural networks have been proposed for glioma grading models, resulting in novel imaging and molecular markers for cancer neuroscience.

PKCζ activation correlates with thyroid cancer aggressiveness and drives malignant progression through EMT regulation. ACPD effectively targets PKCζ-mediated oncogenic pathways, suggesting PKCζ inhibition as a promising therapeutic strategy for aggressive thyroid cancers.

These results suggest that the miR-4664-3p/PRKCB axis is crucial in NSCLC progression and immune modulation. Hence, MiR-4664-3p is a potential diagnostic and prognostic indicator, as well as therapeutic target in immunotherapy strategies for NSCLC.

In comparison, for the 5' UTR variant, rs44582331, no significant association was observed between the mutated genotype (TT) and HCC. Furthermore, functional assays need to be carried out to experimentally validate the role of these UTR variants in cancer pathogenesis.

All five nsSNPs exhibited potential as predictive and prognostic biomarkers for BC. However, the current study findings should be validated by conducting research on large cohorts with representation from diverse population. Furthermore, biological mechanism by which these nsSNPs cause BC pathogenesis could be explored in future studies.

(Z)-endoxifen (endoxifen) is the active metabolite of tamoxifen...In vitro studies in the CRT435 GBM cell line confirmed that endoxifen treatment reduced cell proliferation and induced cell death, while in vivo studies in a subcutaneous CRT435 patient-derived xenograft (PDX) model demonstrated a tolerable safety profile but no significant tumor growth reduction, likely reflecting limitations of the model used. This study underscores the application of AI-driven computational approaches in identifying new therapeutic hypotheses and demonstrates the potential of repurposing endoxifen for GBM treatment.

CREB1 binding to the PRKCH promoter was validated using luciferase reporter assays. Collectively, these findings reveal a novel ROCK1-ERK2-CREB1-PRKCH signaling pathway that coordinates EMT and metabolic reprogramming to drive CRC liver metastasis, highlighting PRKCH as a promising therapeutic target in advanced CRC.

Pharmacologically, the D427N mutant protein displays poor sensitivity to established PKCb inhibitors, necessitating development of bespoke therapeutics for any ATLL intervention through this target. Such efforts could be guided by the availability the D427N mutant-ruboxistaurin structure presented here.

PKCζ may be involved in the progression of ALDH1A3-positive luminal B breast cancer. Furthermore, PKCζ and ALDH1A3 could serve as molecular targets and prognostic biomarkers for predicting the efficacy of endocrine therapy in patients with ALDH1A3 positive luminal B breast cancer.

Single-cell RNA sequencing (scRNA-seq) shows NanoCa increases the population of tumoral infiltrating dendritic cell (DC), C1qc+ TAM, and CD8T_eff cells and decreases the CD8T_ex and immunosuppressive SPP1+ TAM population in tumor-draining lymph nodes. Overall, NanoCa shows translational potential for anti-tumor immune therapeutics.

PKCζ and CTNNBIP1 may serve as a prognostic biomarker for predicting the efficacy of endocrine therapy in the luminal B breast cancer.