Rab11a, Ras-related protein in brain 11A, is a small GTPase and a key regulator in vesicle trafficking, a cellular process crucial for material transport and information delivery. It is involved in multiple biological processes such as endocytic recycling regulation, receptors and adhesion molecules recycling, exosome secretion, phagophore formation, cytokinesis, and also plays roles in several signaling pathways like FAK/AKT and Hippo-YAP [1,3,8].

In cancer research, Rab11a has shown dual characteristics. In gastric, ovarian, prostate, and lung squamous cell carcinomas, its overexpression promotes cell proliferation, invasion, and tumor formation, often via the FAK/AKT signaling pathway. For example, in gastric cancer, Rab11a overexpression increased cell growth, colony numbers, invasion ability, and conferred cisplatin resistance [3]. In ovarian cancer, it promoted malignant progression by inducing autophagy [4]. In prostate cancer, it activated the FAK/AKT signaling pathway to enhance cell malignant progression [5]. In lung squamous cell carcinoma, its expression was associated with cancer aggressiveness through regulation of FGFR-signaling [7]. In colorectal cancer, stress-induced Rab11a-exosomes can induce amphiregulin-mediated cetuximab resistance [2].

In normal physiological functions, newly engineered mouse models (KO/CKO models) revealed that Rab11a, along with Rab11b, redundantly controls mitotic spindle function and intestinal progenitor cell division in the intestinal epithelium [6]. Also, in the colonic epithelium, Rab11a-mediated trafficking is essential for colonic epithelial integrity as it regulates the Hippo-YAP signaling pathway through controlling YAP's localization to adherens and tight junctions [8]. Overall, Rab11a is significant in both normal physiological functions and cancer-related processes, and its study using genetic models has provided valuable insights into these areas.