PARD3 (Par-3 Family Cell Polarity Regulator)

Finally, ensemble machine learning models (mean AUC = 0.839), identified DTNA as the optimal predictive biomarker for distinguishing MASLD from MASH. This study highlight DTNA+ macrophages and the RUNX2-PLG-PARD3 axis as candidate mechanisms and targets for non-invasive diagnosis and therapy in MASH.

Mutations that impair coacervation of RASSF9 or its interaction with PAR3, diminish its promotion of PAR3 phase separation. Our findings identify RASSF9 as a modulator of PAR3 condensates and suggest a phase separation-mediated framework that may contribute to maintaining cell polarity and restraining oncogenic signaling.

The strong concordance between immunohistochemical and transcriptomic profiles-with the exception of DLG7-highlights the disruption of cell polarity as an early and central molecular event in oral carcinogenesis. Collectively, the polarity regulators PAR3, SCRIBBLE, and DLG7 emerge as promising biomarkers for early malignant transformation in oral potentially malignant disorders (OPMDs) and as potential modulators of tumor initiation, progression, and invasive behavior.

We found that Par3L interacts with proteins involved in chromatin remodeling and spindle assemblies, cytoskeleton and extracellular matrix, trafficking, metabolism, and mRNA processing. These data provide valuable information understanding the non-canonical polarity protein Par3L.

Our findings demonstrate that the VPP model, identified through plasma proteomics profiling, serves as a predictive biomarker for response to anti-PD-L1 plus chemotherapy in SCLC patients.

Inhibition of PAR1, PAR2, or PAR4 reduced the viability of adherent GBM cells but not stem-like neurospheres. These findings suggest that PARs impact GBM patient survival and that tumor stem cells may respond differently to PAR inhibition compared to conventional tumor cells.

PDZ proteins may serve as prognostic markers and therapeutic targets in HCC. DEP-related risk scores offer insights into immune infiltration patterns and treatment responsiveness, providing a foundation for future HCC research and development of precision medicine.

Together, these results indicate the role of Par3 in RCC metastasis, via driving metastatic RCC progression by promoting the YAP/TAZ pathway.

In this circuit, the Partitioning defective 3 (Pard3) polarity protein and Junctional adhesion molecule-C (JamC) adhesion molecule promote, while the Seven in absentia 2 (Siah2) ubiquitin ligase inhibits, Deleted in colorectal cancer (Dcc) receptor surface recruitment to gate differentiation linked repulsion to GZ Netrin-1. These results demonstrate cell polarity as a central integrator of adhesive- and guidance cues cooperating to spur GZ exit.

Importantly, cell fitness impairment caused by aPKC depletion is rescued by the restoration of macropinocytosis and aPKCs support PDAC growth in vivo. Our findings enhance our understanding of the mechanistic underpinnings that control macropinocytic uptake in the context of metabolic stress.

In this circuit, the Partitioning defective 3 (Pard3) polarity protein and Junctional adhesion molecule-C (JamC) adhesion protein promote, while the Seven in absentia 2 (Siah2) ubiquitin ligase inhibits, Deleted in colorectal cancer (Dcc) receptor surface recruitment to gate differentiation linked repulsion to GZ Ntn-1. These results demonstrate cell polarity as a central integrator of adhesive- and guidance cues cooperating to spur GZ exit.