ERK1/2-P16(INK4a)Signaling Pathway And MDR1 In Cisplatin Chemoresistance Molecular Omechanisms Of Cervical Adenocarcinoma

To explore the mechanismof P16(INK4a)-ERK1/2 signaling pathway and MDR1(P-gp)involved in cisplatin-resistance of endocervical adenocarcinoma cells formation process.Methods:1.Detection of differentition in expression levels of P16(INK4a)mRNA in Hela and HeLa/DDP cells by fluorescence quantitative PCR2.Detection of proliferation rate of HeLa/DDP cells after transfection of pEX-2P16(INK4a)which is a plasmids after P16(INK4a)overexpressed by cell counting kit-8(CCK-8)technique,and detection of invasion and migration abilities of HeLa/DDP cells after transfection of pEX-2 P16(INK4a)by Transwell technique.3.Detection of changes in expression levels of pERK1/2,ERK1/2 and P-gpprotein after transfection of pEX-2 P16(INK4a)in HeLa/DDP cell by Western Blot.Results:1.The results of qPCR showed the expression levels of P16(INK4a)mRNA in HeLa/DDP groupis lower than in HeLa group(P<0.05).2.The results of CCK8 test showed pEX-2 P16(INK4a)grouphad lower proliferation rate of HeLa/DDP cells compared with HeLa/DDP groupand empty vector control group(pEX-2-empty group)(P<0.05),and there was no statistical significance between HeLa/DDP groupand pEX-2-empty group(P>0.05).3.The results of Transwell test showed pEX-2 P16(INK4a)grouphad lower invasion and migration abilities of HeLa/DDP cells compared with HeLa/DDP groupand pEX-2-empty group(P<0.05),and there was no statistical significance between HeLa/DDP groupand pEX-2-empty group(P>0.05).4.The results of Western Blot showed there was no significant change of total ERK1/2 after transfection of pEX-2 P16(INK4a)in HeLa/DDP cell.The expression level of pERK1/2 protein increased,however,the expression level of P-gpprotein decreased.Conclusion:P16(INK4a)was partially reversed in the cisplatin resistance of cervical adenocarcinoma through ERK1/2 signaling pathway phosphorylation.