RAB35 (RAB35, Member RAS Oncogene Family)

These results emphasize the challenges of interfering with EV secretion, as several parallel pathways, such as direct membrane budding, can compensate. Further studies are needed to develop models for studying the role of EVs in vivo.

Focusing on two inhibitors, we demonstrate the inhibition of K-Ras in downstream signaling and cellular proliferation in human pancreatic and non-small cell lung cancer cells expressing wild-type or mutant K-Ras. These two compounds represent novel pan-Ras superfamily inhibitors as they also inhibited GTP binding to other members such as RAB5A and RAB35.

Notably, migrasomes hold promise as diagnostic biomarkers, especially in early podocyte injury, and as therapeutic targets in oncology and regenerative medicine. This review summarizes the current understanding of migrasome biology, and their implications in health and disease, and explores emerging perspectives on harnessing migrasomes for diagnostic and therapeutic applications.

Furthermore, overexpression of related Rab proteins with overlapping functions does not rescue the cytokinetic defects caused by Rab11 or Rab35 downregulation in cancer cells. Therefore, this study aims to deepen our understanding of how Rab11 and Rab35 orchestrate the molecular events that drive the progression from late anaphase through the completion of cytokinesis.

While the results are preliminary due to the sample size, this study is the first to identify circHOTAIR as both a prognostic and diagnostic biomarker in B-ALL. Furthermore, it elucidates the role of HOTAIR as a sponge for miR-326, orchestrating its efflux from the cell via exosomes through RAB35.

These differential proteins offer potential new candidate molecules for further research on the pathogenesis of mCRC and the identification of therapeutic targets. This study sheds light on the potential significance of plasma exosome proteomics studies in our understanding and treatment of mCRC.

The use of Rab35 dominant negative mutant is proposed for functional in vivo studies on the roles of native EVs. Ultimately, investigations on native EVs will tremendously advance our understanding of EV biology and open novel opportunities for therapy and prevention.

In contrast, Rab7a shows low colocalization with LC3 puncta and low level in the autophagosome, suggesting it regulates different vesicle trafficking machineries. Our findings open a new direction toward exploring the role of Rab proteins in secretory autophagy-related cargo exocytosis and identifying the cargoes and effectors regulated by specific Rab proteins.

Importantly, variant expression leads to delayed cytokinesis and altered length, number, and Arl13b composition of primary cilia, known factors in neurodevelopmental disease. Our findings provide evidence of altered Rab35 function as a causative factor of a neurodevelopmental disorder.

Our study provides new insights into the biological activities of DG in lung cancer cells, contributing to the development of novel oncological therapies.

Finally, the angiogenesis-promoting effect of JAG1 in TNBC was further investigated by matrix gel assay. In conclusion, we reveal that JAG1 has a pro-invasion effect on TNBC and is involved in microenvironment angiogenesis by promoting exosome secretion and the MALAT1-miR-140-5p-JAG1/VEGFA pathway.

Moreover, up-regulation of the exosome markers TSG101, Alix, and CD63 as well as down-regulation of tumor-suppressive miR-200b and miR-200c were observed in exosomes derived from DDX3-knockdown HCC cells, which may account for the enhanced hepatic cancer stemness of the recipient cells treated with DDX3-knockdown HCC cell-derived exosomes. Taken together, our findings provide a new molecular mechanism supporting the tumor-suppressor role of DDX3 in HCC, which may contribute to the development of new therapeutic strategies against HCC.