KIF3A Inhibits The Ability Of Invasion,migration And Proliferation In Nasopharyngeal Carcinoma By Regulating Wnt/?-catenin Signaling Pathway

Research Background and PurposesNasopharyngeal carcinoma(NPC)is an epithelial malignant tumor originated from the lining of the nasopharyngeal mucosa.NPC geographical distribution is extremely unbalancedin the world.More than 70%of new cases occur in East Asia and Southeast Asia,with obvious regional and ethnic differences.Early-stage nasopharyngeal carcinoma can be cured by radiotherapy alone,while advanced nasopharyngeal carcinoma requires combined radiotherapy and chemotherapy to achieve a relatively better prognosis.Therefore,it is very important to explore the biomarkers for early diagnosis of nasopharyngeal carcinoma.KIF3A is one of the components of primary cilia,which can mediate the transduction of multiple signal pathways.The loss of primary cilia was found in a variety of tumors,suggesting that primary cilia plays an important role in tumors.KIF3 A is involved in the formation of kinesin 2 in the primary cilia,and its deletion can lead to the obstruction of the hair growth process of the primary cilia.Many studies have found that KIF3 A can regulate tumorigenesis and development through Wnt signaling pathway,but its role in nasopharyngeal carcinoma has not been reported yet.Research MethodThis study first explored the expression of KIF3 A in nasopharyngeal carcinoma through immunohistochemical staining,and studied the relationship between KIF3A and the classification,grading and staging of nasopharyngeal carcinoma.Subsequently,the effect of KIF3A on the invasion,migration and proliferation of nasopharyngeal carcinoma was explored through Transwell experiment,Wound healing experiment,CCK8 experiment,EDU experiment,and tumor formation in nude mice experiment.Finally,the Western blot experiment was used to further explore the molecular mechanism of KIF3A's influence on the invasion,migration and proliferation of nasopharyngeal carcinoma.Research ResultIn this study,immunohistochemical staining confirmed that the expression of KIF3A in nasopharyngeal carcinoma was lower than that of normal mucosal tissues,and the expression of KIF3A was negatively correlated with T-staging and M-staging.Subsequent Transwell experiment,Wound healing experiment,CCK8 experiment,EDU experiment and tumor formation in nude mice experiment found that the ability of invasion,migration and proliferation in nasopharyngeal carcinoma cells overexpressing KIF3A was inhibited.Further molecular mechanism studies have found that KIF3A may regulate the Wnt/?-catenin signaling pathway through phosphorylation of GSK3? Ser9 site,and then affect the expression of Epithelial-Mesenchymal Transition(EMT)and cycle-related proteins to inhibit the invasion,migration and proliferation of nasopharyngeal carcinoma cells.Research ConclusionKIF3A can be used as a potential diagnostic and therapeutic target for nasopharyngeal carcinoma,and it may exert a tumor suppressor effect through Wnt/?-catenin signaling.