CD109 facilitates progression and 5-fluorouracil resistance of nasopharyngeal carcinoma

Abstract

CD109 involves in human cancers, but its role and mechanism in the chemosensitivity of nasopharyngeal carcinoma (NPC) cells is yet to be investigated. Our investigation discovered that the CD109 had abnormally higher expression in the NPC tissues and cells. By depleting or supplementing CD109 in the NPC cells, the aggressive capabilities of NPC cells were suppressed or augmented, respectively. Moreover, silencing of CD109 promoted NPC cells chemosensitivity to 5-FU, and also inhibited 5-FU-mediated cell biological behaviors, facilitating cell apoptosis. Furthermore, CD109 was found to regulate the activities of AKT/mTOR signaling in the NPC cells. The tumor-promotive effect of CD109 overexpression was partially annulled by AKT/mTOR signaling inhibition. Finally, we also observed that tumor growth was retarded in the xenograft mice model and activity of AKT/mTOR signaling was reduced in the CD109 deficient group. Our data indicated that CD109, could be a therapeutic biomarker candidate in NPC treatment.