The Mechanism Of Long Non-coding RNA Uc002ktr.3 On Drug Resistance To Cisplatin In Lung Squamous Cell Carcinoma

Objectives To investigate the role and mechanism of long non-coding RNA uc002ktr.3（lnc-uc002ktr.3）in cisplatin resistance of lung squamous cell carcinoma.Methods（1）RACE experiment and Sanger sequencing were used to obtain the lnc-uc002ktr.3 full-length sequence;Nucleoplasmic separation assay to determine the location of the cells;（2）CCK-8 assay,flow cytometry and Western blot were used to detect the down-regulated expression of lnc-uc002ktr.3 on cisplatin in lung squamous cell carcinoma cells respectively,including IC₅₀0 change,apoptosis rate change and expression of apoptosis-related protein（Bax,cleaved PARP）,so as to clarify the role of lnc-uc002ktr.3in cisplatin resistance of lung squamous cell carcinoma.（3）The effect of down-regulated lnc-uc002ktr.3 expression on Mib1 expression,Wnt/β-catein signaling pathway and EMT was determined by qRT-PCR and Western blot,to reveal the mechanism of lnc-uc002ktr.3 in cisplatin resistance of lung squamous cell carcinoma.Results（1）RACE sequencing showed that lung squamous cell carcinoma lnc-uc002ktr.3 contained only one exon,lacked open reading frame,and had no protein-coding function.Its total length was 688 nt,mainly distributed in the nucleus.（2）After interfering with uc002ktr.3 combined with cisplatin in vitro,it was found that IC₅₀0 of lung squamous cell carcinoma cells was significantly reduced,apoptosis rate was significantly increased,and expression of apoptotic protein Bax and cleaved PARP were also significantly increased.（3）In lung squamous cell carcinoma cells,interference with uc002ktr.3 expression can inhibit the expression of Mib1 protein.（4）In lung squamous cell carcinoma cells,interference with uc002ktr.3 expression can inhibit the Wnt/β-catenin signal pathway.Conclusions Stable and highly expressed lnc-uc002ktr.3 in lung squamous cell carcinoma cells can significantly promote the formation of cisplatin resistance in lung squamous cell carcinoma cells,which can mediate cisplatin resistance in lung squamous cell carcinoma cells by activating the Wnt/β-catein signaling pathway and promoting EMT.Therefore,lnc-uc002ktr.3 is expected to be an important molecular target for the treatment of cisplatin resistance in lung squamous cell carcinoma.