Abstract
Less than a century ago, gastric cancer (GC) was the most common cancer throughout the world. Despite advances in surgical, chemotherapeutic, and radiotherapeutic treatment, GC remains the number 3 cancer killer worldwide. This fact highlights the need for better diagnostic biomarkers and more effective therapeutic targets. RAB11-FIP2, a member of the Rab11 family of interacting proteins, exhibits potential tumor suppressor function. However, involvement of RAB11-FIP2 in gastric carcinogenesis is yet to be elucidated. In this study, we demonstrated that RAB11-FIP2 was downregulated in GC tissues and constituted a target of the known onco-miRs, miR-192/215. We also showed that functionally, Rab11-FIP2 regulation by miR-192/215 is involved in GC-related biological activities. Finally, RAB11-FIP2 inhibition by miR-192/215 affected the establishment of cell polarity and tight junction formation in GC cells. In summary, this miR-192/215–Rab11-FIP2 axis appears to represent a new molecular mechanism underlying GC progression, while supplying a promising avenue of further research into diagnosis and therapy of GC.
Highlights
Gastric cancer (GC) is the third-most common cause of cancer death worldwide, there are approximately 951,600 new GC cases and 723,100 deaths every year[1]
Decreased expression and potential tumor-suppressive function of Rab11- FIP2 in GC Expression levels of Rab11-FIP2 were measured in 45 paired tumor tissue specimens from GC patients by real-time reverse transcription polymerase chain reaction (RT-PCR)
Rab11-FIP2 protein expression levels were assayed by immunohistochemistry (IHC) in a GC tissue microarray
Summary
Gastric cancer (GC) is the third-most common cause of cancer death worldwide, there are approximately 951,600 new GC cases and 723,100 deaths every year[1]. The Rab11-family interacting proteins (Rab11-FIPs), which comprise at least six mammalian genes, Rip[11], Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, RCP, and Rab11FIP4, are well-documented participants in the regulation of apical membrane recycling and transcytosis in epithelial cells[4]. Rab11-family interacting protein 2 (Rab11FIP2) forms a ternary complex with Rab[11] and the motor protein myosin Vb to regulate basolateral-toapical transcytosis in MDCK(Madin-Darby canine kidney) cells[5,6]. The complex of Rab11-FIP2/Rab11a/myosin Vb participates in Rab11-mediated recycling pathways[5]. Naslavsky et al.[7] showed that Rab11-FIP2 and Eps[15] homology domain (EHD) 1 acted in a coordinated fashion to mediate early endocytic recycling. To date, emerging evidence shows that Rab11-FIPs are involved in tumor progression and metastasis. The participation of Rab11-FIP2 in human gastric carcinogenesis
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