RAB26 Promotes Nasopharyngeal Carcinoma Cell Proliferation through Activation of β-catenin Signaling
This study explored the effect of RAB26 on nasopharyngeal carcinoma cell proliferation and its underlying mechanism.The RAB26 mRNA and protein expression levels in nasopharyngeal cancer tissues and normal nasopharyngeal epithelial tissues were detected by real-time fluorescence quantitative PCR and immuno-histochemistry experiments,and statistical analyses of RAB26 expression levels evaluated by immunohistochem-istry with the clinicopathological characteristics of patients.RAB26 was overexpressed in nasopharyngeal carci-noma CNE-2 cells and knocked down in HNE1 cells,and overexpressed and knocked down cell lines were established respectively.The impact of RAB26 on the proliferation of the NPC cells was detected by CCK-8 proliferation assay,cell clone formation assay and EdU proliferation assay.Western blot assay was used to detect the protein expression levels of RAB26,β-catenin,cyclinD1,c-Myc and survivin in Wnt/β-catenin signaling and p-p3 8 MAPK/p38 MAPK,p-ERK/ERK in MAPK/ERK signaling in nasopharyngeal carcinoma cells with overexpression and knockdown of RAB26.The CNE-2 overexpressed RAB26 cell viability after X-ray irradiation with different irradiation doses(0 Gy,2 Gy,4 Gy,6 Gy and 8 Gy)was detected in the cell clone formation assay.The results showed that RAB26 was highly expressed in naso-pharyngeal carcinoma.The expression level of.RAB26 in nasopharyngeal carcinoma was positively correlated with the tumor type(r=0.294,P＜0.05)and metastasis/recurrence(r=0.290,P＜0.05).After overexpression of RAB26,CNE-2 nasopharyngeal carcinoma cells showed accelerated proliferation,increased expression of β-catenin,cyclin D1,c-Myc,and survivin proteins,and increased expression of p-p38 MAPK,p-ERK proteins,while the opposite was observed after knockdown of RAB26.Reduced radiosensitivity of nasopharyngeal carcinoma cells by overexpres-sion of RAB26.In conclusion,RAB26 showed high expression in nasopharyngeal carcinoma and promoted the pro-liferation of nasopharyngeal carcinoma cells by activating the Wnt/β-catenin signaling pathway and the MAPK/ERK signaling pathway.
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