CDC42 (Cell Division Cycle 42)

Clinically, ROLLCSC and its targets are associated with distinct tumor expression patterns and have prognostic significance. Overall, our study elucidates how the lncRNA ROLLCSC derived from cancer stem cell (CSC)-derived EVs is efficiently transported to LUAD cells, subsequently reshaping the lipid metabolism of recipient cells and enhancing their resistance to ferroptosis.

To encapsulate our findings, we have determined eight MAPK pathway-associated CRC prognostic biomarkers and developed a prognostic model accordingly. This model has proven effective in stratifying the risk levels among CRC patients.

Collectively, we identified a previously unreported molecular mechanism underlying functional impairment of NK cells from older adults. In perspective, our data hold promise to develop novel strategies against age-related disorders driven by tissue-resident senescent fibroblasts.

Immunohistochemical analysis did not uncover astrocyte or microglial activation, implying that myelin outfoldings per se do not induce secondary neuropathology. Together, our data reveal a critical function for CDC42 and CDC42EP1/CDC42EP2 in regulating myelin septin filaments, which facilitate structural integrity of myelin sheaths.

In vivo, mice injected with tumor cells pre-cultured on high-stiffness ECM-mimicking hydrogels exhibited accelerated subcutaneous tumor growth and increased lung metastatic burden, which were significantly attenuated by FAK-targeted therapy. These findings establish ECM stiffness as a biomechanical determinant of ATC progression and metastasis, offering novel insights into microenvironment-driven malignancy and highlighting FAK as a promising therapeutic target to disrupt mechanosignaling in ATC.

Architecturally more complex forms within this spectrum exist and have been labelled as having "uncertain malignant potential." Malignant mesothelioma of the tunica vaginalis is an uncommon but aggressive tumor that may show loss of BAP1 or MTAP immunostaining, supporting a distinct molecular pathogenesis. This review summarizes the clinicopathologic, immunohistochemically, and molecular features of mesothelial lesions of the paratestis, emphasizing their morphologic overlap, diagnostic pitfalls, and evolving framework for classification.

The Y64C variant disrupts neurite outgrowth, attributable to altered CDC42 activity and localization. The restoration of neurite outgrowth by GGTI-298 highlights the importance of CDC42 signaling for neurite outgrowth in Neuro2A cells. Our findings raise the possibility that molecular disruptions caused by the Y64C mutation may contribute to the brain malformations and neurodevelopmental features observed in TKS.

Collectively, these findings highlight persistent gaps, including limited integration with immuno-oncology and precision medicine frameworks and underexplored roles of non-canonical Rho GTPases. This bibliometric assessment provides a structured overview of three decades of research and identifies priorities to guide future investigations into Rho GTPase-driven cancer biology and therapy.

CircPTPRM can encode circPTPRM-187aa polypeptide. circPTPRM-187aa, regulates the expression of IQGAP1 protein, and up-regulates RAC1 and CDC42 proteins in TGF-β signaling pathway, enhancing the PTC cells proliferation, migration, and invasion.

We also find that THSD7A induces filopodia formation through activation of the Rho GTPase, Cdc42. These findings suggest a new model for filopodia formation, triggered by exosomes carrying THSD7A.

This activates phosphatidylinositol-4-phosphate-5-kinase (PI5K) to increase local phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) levels, promoting actin-polymerization and membrane protrusion. Therefore, CD13 is a novel molecular PIP regulator, modulating signal transduction and downstream cellular processes, including actin cytoskeleton dynamics and membrane organization to facilitate intercellular communication.