RAB32 (RAB32, Member RAS Oncogene Family)

The gene signature developed provides a reliable tool for prognosis and may inform personalized treatment. This SPP1+ macro-associated signature offers a novel and robust biomarker for prognosis and may guide precision immunotherapy strategies in HCC.

This study developed a multi-omics-integrated prognostic model (LMS) based on lactate metabolism, providing a novel tool for risk stratification and therapeutic decision-making in SKCM patients. It also identified RAB32 as a central player in tumor metabolic reprogramming and invasiveness, with promising potential as a therapeutic target.

Finally, Rab32 AKAP function and OPTN phosphorylation are required for Golgi repositioning during cell migration, contributing to tumor cell invasion. Together, these data reveal a role for Rab32 in regulating Golgi dynamics through PKA-mediated phosphorylation of OPTN.

Knocking down the expression of the RAB32 gene significantly inhibited the proliferation, migration and invasion of glioma cells. Our results show that RAB32 is a key factor affecting the prognosis of patients with GBM, and its targeting may provide a new treatment for patients with GBM.

RAB32 promotes malignant progression of glioblastoma cells through the JAK/STAT signaling pathway, providing new possibilities for therapeutic targets for glioblastoma.

The risk model associated with pyproptosis is crucial for the tumor immunity of LC and may serve as a prognostic indicator for patients suffering from LC. Our findings will offer new perspectives for immunotherapies targeting LC.

Inactivation of both LYSMD1 and LYSMD2 reduces Rab32 activation, causing melanosome enlargement and decreased melanin production in mouse melanoma cells. These findings provide important mechanistic insights into LRO biogenesis and functions.

This risk model was closely associated with the immune infiltration microenvironment. The four key VMTRGs are powerful prognostic biomarkers and therapeutic targets for LIHC.

Our findings reveal that PIK3CD expression is associated with prognosis, EMT, and tumor immune infiltration in BRCA patients.

Deletion or mutation of LRRK2's Rab38 binding site in the N-terminal armadillo domain decreases LRRK2 membrane association, pericentriolar recruitment, and ability to phosphorylate Rab10. In sum, our data identify Rab38 as a physiologic regulator of LRRK2 function and lend support to a model in which LRRK2 plays a central role in Rab GTPase coordination of vesicular trafficking.

Schematic of Rab32 promotes GBM aggressiveness via regulation of ERK/Drp1-mediated mitochondrial fission. Rab32 transports Drp1 from the cytoplasm to the mitochondria and recruits ERK to activate the ser616 site of Drp1, which in turn mediates mitochondrial fission and promotes mesenchymal transition, migration and invasion of GBM.