Rab11a, the Ras-related protein in brain 11A, is a small GTPase that serves as a key regulator in vesicle trafficking, a cellular process crucial for material transport and information delivery. It is involved in multiple biological pathways, such as endocytic recycling regulation, receptors and adhesion molecules recycling, exosome secretion, phagophore formation, cytokinesis, and Hippo-YAP signaling pathway [1,8]. Dysregulation of Rab11a has been associated with various diseases, especially cancers [1].

In mouse models, compound ablation of Rab11a and Rab11b leads to defective cell cycle entry, mitotic arrest, and apoptosis in intestinal epithelial progenitor cells, uncovering their redundant role in controlling mitotic spindle function and cell division [6]. In human studies, Rab11a is overexpressed in gastric, ovarian, and prostate cancers, promoting cell proliferation, invasion, and autophagy, and conferring drug resistance [3,4,5]. In colorectal cancer, stress-induced Rab11a-exosomes can induce cetuximab resistance [2]. In lung squamous cell carcinoma, its expression is associated with cancer aggressiveness through regulation of FGFR-signaling [7].

In conclusion, Rab11a is essential in vesicle-related biological processes. The study of Rab11a knockout or conditional knockout mouse models has provided insights into its role in maintaining tissue homeostasis, especially in the intestinal epithelium. In disease areas, research on Rab11a has highlighted its significance in cancer development and progression, suggesting it could be a potential therapeutic target.