RhoB, a member of the Rho family GTPases, shares high sequence similarity with RhoA and RhoC but has distinct functions. It is involved in multiple cellular processes such as actin organization, cell migration, membrane trafficking, cell proliferation, DNA-repair, and apoptosis. RhoB interfaces with pathways like EGFR, Ras, and PI3K/Akt to modulate cellular responses [3,4].

In colitis, RhoB shows increased expression in ulcerative colitis (UC) patients and DSS-induced colitis mice. RhoB+/- and RhoB-/- mice have milder DSS-induced colitis, with increased goblet cell numbers and IEC proliferation. Decreased RhoB promotes goblet cell differentiation and epithelial regeneration by inhibiting the Wnt signaling pathway and activating the p38 MAPK signaling pathway. Additionally, these mice have increased SCFA-producing bacteria, SCFA concentrations, and upregulated SCFA receptor expression, suggesting RhoB as a potential biomarker and treatment target for UC [1]. In pancreatic cancer, RhoB is down-regulated in gemcitabine-resistant cells, and it is a downstream target of hsa-miR-3178. RhoB can reverse hsa-miR-3178-mediated gemcitabine resistance, and the hsa-miR-3178/RhoB/PI3K/Akt pathway regulates ABC transporters related to gemcitabine resistance [2].

In conclusion, RhoB has diverse functions in regulating cellular processes. The study of RhoB using gene knockout mouse models has revealed its role in diseases like colitis and pancreatic cancer. These findings provide insights into the potential of RhoB as a biomarker and therapeutic target, contributing to a better understanding of disease mechanisms and paving the way for new treatment strategies.