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The Study On PLUNC Regulating EMT In Nasopharyngeal Carcinoma Cells Through NLRP3 Inflammasome

Posted on:2023-11-02Degree:MasterType:Thesis
Country:ChinaCandidate:Y B QiuFull Text:PDF
GTID:2544307070997939Subject:Clinical Laboratory Science
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Objective: To investigate whether NLRP3 inflammasome can regulate EMT,proliferation ability,and the expression of PD-L1 of NPC cells and whether NLRP3 inflammasome is involved in the regulation of EMT and PD-L1 expression of NPC cells by PLUNC.Methods: Two nasopharyngeal carcinoma cell lines S26 and S18 were treated with LPS,ATP and LPS,ATP,and MCC950 at the same time,and the activation of the NLRP3 inflammasome,EMT related molecules,proliferation,and expression of PD-L1 were detected.After lentivirusoverexpressing NLRP3 was transfected into S26 and S18,the proliferation and migration of nasopharyngeal carcinoma cells were detected.Overexpression of LV-PLUNC in S26 and S18 cells,S26 and S18 overexpressing PLUNC lentivirus were treated with LPS and ATP;the activation of the NLRP3 inflammasome,EMT related molecules,and the expression of PD-L1 was detected.Results: The expressions of NLRP3 and IL1β p17 of two nasopharyngeal carcinoma cell lines S26 and S18 were up-regulated after LPS combined with ATP treatment,and membrane perforation increased under the electron microscope.Moreover,the protein levels of NLRP3,IL1β p17 in two nasopharyngeal carcinoma cell lines S26 and S18 were down-regulated after LPS,ATP,and MCC950 treatment,indicating that the NLRP3 inflammasome was activated after LPS combined with ATP treatment,and PLUNC could inhibit its activation.Overexpression of NLRP3 promoted the proliferation of nasopharyngeal carcinoma cells S26 and S18,while transfection of the lentivirus-overexpressing PLUNC inhibited the proliferation of nasopharyngeal carcinoma cells and downregulated the expression of N-cadherin,cyclin D1,and PD-L1.LPS and ATP treatment promoted proliferation of nasopharyngeal carcinoma cells S26 and S18,and up-regulated the expression of N-cadherin,Vimentin,cyclin D1,PD-L1,and other molecules;while LPS,ATP,and MCC950 treatment at the same time reduced the above molecular levels.These results suggested that the activation of NLRP3 inflammasome can promote EMT,proliferation,and the expression of PD-L1 in NPC cells S26 and S18,while overexpressing PLUNC can inhibit EMT and the expression of PDL1 of NPC cells S26 and S18 induced by the activation of the NLRP3 inflammasome,suggesting that NLRP3 inflammasome may be involved in PLUNC regulating EMT and the PD-L1 expression and of NPC cells.Conclusion: 1.The NLRP3 inflammasome activation could promote EMT,the expression of PD-L1,and the proliferation of NPC cells.2.Overexpression of PLUNC can inhibit the NLRP3 inflammasome activation,and inhibit EMT and the expression of PD-L1 in nasopharyngeal carcinoma cells induced by NLRP3 inflammasome activation.Figures14,Tables 8,References 81...
Keywords/Search Tags:Nasopharynx cancer, PLUNC, NLRP3 inflammasome, EMT, PD-L1
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