Investigation Of Centripetal Assembly Protein STIL Knockdown In The Treatment Of Nasopharyngeal Carcinoma

Nasopharyngeal carcinoma(NPC)is an epithelial carcinoma occurring in the lining of the nasopharyngeal mucosa.The onset is mostly caused by multiple factors such as EBV infection,genetic susceptibility,and environment.The global distribution of nasopharyngeal cancer is extremely uneven.Although the incidence and mortality rate of nasopharyngeal cancer are gradually decreasing,nasopharyngeal cancer is still one of the most common primary malignant tumors in China.At present,the treatment of nasopharyngeal carcinoma is mainly based on radiotherapy and chemotherapy,supplemented by molecular targeted therapy and immunotherapy.The combination of radiochemotherapy and molecular targeted therapy has significantly improved the survival rate of patients with advanced nasopharyngeal carcinoma,suggesting the important role of our molecular targets in the treatment of nasopharyngeal carcinoma.Some regulatory networks involving nasopharyngeal carcinoma have been reported,but related genes have not yet been fully determined.In the previous study,we used the m RNA chip to identify 20 genes that may play an important role in the proliferation of nasopharyngeal carcinoma.High-throughput sh RNA screening and q PCR verification results showed that STIL had the greatest effect on the proliferation rate of nasopharyngeal carcinoma cells.STIL knockdown CNE-2Z cell biological characteristics analysis results showed that STIL knockdown inhibited cell proliferation and induced apoptosis,and affected the cell cycle.This essay further studies the effects of STIL on the proliferation,invasion and distant metastasis of nasopharyngeal carcinoma,which may help to develop new treatment strategies targeting STIL or more accurate prognosis prediction.Based on the previous research,we analyzed the relationship between the STIL gene and a variety of tumor types in the public database of The Cancer Genome Atlas(TCGA),and further verified the previous conclusions at the animal level.Then,CNE-2Z cells with STIL knockdown were tested by m RNA chip,detecting the expression of STIL-related differential genes and the ability of cell invasion and migration.The serum of nasopharyngeal carcinoma metastasis samples was also detected by DIA mass spectrometry and ELISA for the expression differential proteins.The results are as follows: 1)TCGA data shows that STIL is up-regulated in a variety of tumors,and high expression is associated with poor prognosis;2)BALB/c mice tumorigenesis experiments show that STIL knockdown does effectively inhibit the proliferation of tumors;3)Transcriptome analysis,q PCR and Western Blot experiments showed that the three genes related to tumor molecular mechanisms(ITGA2,SMAD2,JAK1)and the two genes related to tumor metastasis and invasion(CD44,ITGAV)were all affected by STIL downregulation;4)Transwell invasion and migration experiments show that the down-regulation of STIL can effectively inhibit the migration and invasion of nasopharyngeal carcinoma cells;5)DIA mass spectrometry analysis show that there are several differential proteins in the serum of nasopharyngeal carcinoma metastasis samples,but the results of ELISA are inconsistent with DIA mass spectrometry data analysis results,and further verification is needed later.In conclusion,our research confirms that STIL is a key regulatory factor that promotes the proliferation,metastasis and invasion of nasopharyngeal carcinoma.It provides ideas for the molecular mechanism research of nasopharyngeal carcinoma and proposes a new treatment strategy.