RAB1A (RAB1A, Member RAS Oncogene Family)

Finally, we show that RAB1A expression reshapes the surfaceome by increasing the abundance of plasma membrane proteins associated with poor overall survival in UM, highlighting its potential as a biomarker. This study identifies protein vesicle transport as an unrecognized vulnerability in UM and supports a mechanistic rationale for targeting MNK1/2 and mTOR in metastatic UM.

Our findings elucidated the detailed mechanism by which mTOR/RAB1A regulates EV secretion, providing new insight into cellular changes involved in PMN formation and a theoretical basis for the inhibition of the PMN in the development of targeted therapies for PCa. RAB1A represents a therapeutic target to reverse tEV-mediated immunosuppression, while peripheral B-cell dynamics provide diagnostic biomarkers for early metastasis detection.

Furthermore, RAB1A facilitated HBV replication by triggering ULK1-mediated autophagy by interacting with C9orf72. In conclusion, RAB1A enhances HBV replication through dual synergistic mechanisms at the transcriptional and post-transcriptional levels, positioning RAB1A as a potential novel target for the treatment of chronic HBV infection.

Rab1A overexpression was associated with poor prognosis and adverse clinicopathological parameters in cancer patients and had the potential to be a target for future cancer therapy.

Finally, nomograms revealed the overall 3 and 5-year survival determined crucial roles of Rab1A/IL-4Rα expression in predicting the prognosis of GC patients. Therefore, Rab1A/IL-4Rα is vital in GC, providing a novel perspective on targeted GC therapy.

In conclusion, our findings concluded that SGOL2 stabilized RAB1A expression to promote prostate cancer development. Both of them were of great importance in TME modulation.

The study on circ_002136 provides good data to support our insight into the mechanism of to-be-silenced circRNA as a therapeutic agent in the progression of HCC.