We found that cytohesin-2 was more highly expressed in HCC compared to adjacent non-tumorous liver tissues, and cytohesin-2 expression was significantly increased in specimens with high α-fetoprotein and vascular invasion.
Arf6 and its GEFs facilitated membrane ruffling and pathogen invasion via ARNO, and triggered actin assembly by generating an Arf1-WRC signaling hub at the membrane in vitro and in cells.
Inhibition of cytohesin-2 by SecinH3 reduces growth of EGFR-dependent lung cancer xenografts and improves the treatment of primarily EGFR-TKI-resistant lung cancers.
In conclusion, cytohesin-2 may identify low-and high-risk individuals with HCC and may be a valuable indicator for stratifying prognosis of TNM stage I patients.