To Investigate The Expression And Prognostic Correlation Of LECT2 In Non-small Cell Lung Cancer Based On TCGA Database

Background&Objective:Leukocyte cell-derived chemokine 2(LECT2),a secreted protein,was originally identified as a chemotactic factor for neutrophils,which is a multifunctional protein that plays an important role in inflammation,immunity,metabolism and tumor.Many studies have shown that LECT2 can suppress the development and metastasis of hepatocellular cancer.However,whether LECT2 plays a similar role in the lung cancer remains unclear.This study aims to examine the expression of LECT2 in non-small cell lung cancer(NSCLC)and to investigate its significance and potential mechanism in the prognosis of NSCLC.Methods:Firstly,using Perl script language to perform the genetic transformation and using R language to extract LECT2 gene expression after downloading the NSCLC transcriptome raw data in TCGA database website.Secondly,Wilcoxon rank was used to analyze the expression differences in cancer tissue and the adjacent tissues of carcinoma,Wilcoxon rank,chi-square,and Univariate(Multivariate)logistic regression analysis method were used to explore the relationship between LECT2 expression and patients’ clinical parameters or the pathological features.Thridly,Univariate(Multivariate)Cox regression model and Kaplan-Meier(K-M)survival analysis were used to analyze the relationship between the expression of LECT2 and the 5-year survival rate of NSCLC patients and the potential mechanism of LECT2 in the development of NSCLC was explored by GSEA enrichment analysis.Finally,the concentration of LECT2 in serum of healthy control group and NSCLC was detected by ELISA and the expression of LECT2 protein in lung tissue of control group and NSCLC was detected by IHC to confirm the expression of LECT2 in NSCLC.Cck8 was used to detect the effect of LECT2 on the proliferation of A549 cells to verify the role of LECT2 in NSCLC.Results:1.The analysis of TCGA database showed that the expression of LECT2 in NSCLC tumor tissues was higher than in adjacent tissues(P<0.05),and the expression level of LECT2 was not significantly different considering genders,ages,primary tumor,lymph node metastasis,distant metastasis and stages(P>0.05),but there were significant differences in the histological types of lung cancer(P<0.05),the expression level of LECT2 in lung squamous carcinoma tissues was significantly higher than in lung adenocarcinoma tissues.2.Univariate(Multivariate)Cox regression model and K-M survival analysis showed that LECT2 could affect the 5-year survival rate of the patients with lung squamous carcinoma and those patients who testified LECT2 positive had a higher 5-year survival rate than negative group(P<0.05).3.GSEA gene enrichment analysis showed that there were 8 pathways in the LECT2-upregulated group,such as P53 signaling pathway and Hedgehog signaling pathway.There were 19 pathways in the LECT2-downregulated group,including cytokine-cytokine receptors,leukocyte transendothelial migration and cell adhesion molecules.4.The ELISA results of serum showed that LECT2 levels in NSCLC patients were higher than those in healthy controls(P<0.05),and the results of lung tissue IHC analysis showed that the expression of LECT2 in NSCLC group was significantly higher than that in control group(P<0.05).CCK8 test results show that LECT2 can inhibit the proliferation of A549 cells.Conclusions:1.The expression of LECT2 in tumor tissues was significantly higher than in adjacent tissues or control group,but there was no difference considering genders,ages,primary tumor,lymph node metastasis,distant metastasis,and stages.In short,LECT2 may be a potential biomarker for NSCLC.2.LECT2 affects the 5-year survival rate of lung squamous cell carcinoma.The 5-year survival rate of patients with lung squamous cell carcinoma in the LECT2-positive group was significantly higher than that in the negative group(P<0.05).3.LECT2 regulates the occurrence and development of non-small cell lung cancer by promoting the P53 signaling pathway,inhibiting cytokine-cytokine receptor interaction,leukocyte transendothelial migration and cell adhesion molecule adhesion.