SQLE Promotes Lung Cancer Cells Proliferation By Regulating ERK Pathway

Background and purposeAt present,the incidence of lung cancer is at the top of global cancer,and the mortality rate of lung cancer in China has increased significantly.It has become the leading cause of cancer death.Among them,lung squamous cell carcinoma accounts for about 30% of lung cancer and may have no obvious symptoms at an early stage.Therefore,biomarkers occupy an important position in the early detection,early diagnosis,and early treatment of lung squamous cell carcinoma.A number of previous studies have shown that there is a close relationship between the occurrence and development of cancer and cholesterol metabolism.Squalene cyclooxygenase(SQLE)is present in the endoplasmic reticulum and is one of the key rate-limiting enzymes in the first step of cholesterol biosynthetic oxidation.Previous studies have found that SQLE has a close relationship with the occurrence and development of various tumors such as liver cancer,breast cancer,colorectal cancer,and bladder cancer.Previous studies have reported that the expression level of SQLE in lung squamous cell carcinoma is significantly higher than that in paracancerous tissues,and the prognosis of patients with lung cancer has a certain correlation with the gene by analyzing the survival period of patients and the expression level of SQLE,but the occurrence of lung squamous cell carcinoma is related to SQLE.The mechanism for development is not yet clear.This experiment applied bioinformatics technology to analyze the effect of SQLE on the prognosis of patients and explore its mechanism of promoting the proliferation of lung squamous carcinoma cells.Research methodsGene Expression Omnibus(GEO)analysis was used to compare gene expression differences in lung squamous cell carcinoma and its adjacent tissues.Then use Oncomine online database to compare the expression of SQLE in lung adenocarcinoma,lung squamous cell carcinoma,small cell lung cancer and lung benign tumor.Kaplan-Meier survival curves were then used to analyze the relationship between the expression level of SQLE and the survival time of squamous cell carcinoma patients.The si-RNA was transfected into lung squamous carcinoma cell H520 using cationic liposome transfection method to silence the expression of SQLE.Total RNA and total protein in transfected H520 cells were extracted by Trizol method and RIPA cell lysate,and then the m RNA and protein levels of p ERK1/2 were detected by RT-PCR and Western-blot techniques from RNA and protein levels,respectively.The expression level.At the same time,MTT assay was used to detect the growth of lung squamous carcinoma cells after transfection.Research resultThrough analysis of the GEO database,342 differentially expressed genes were identified,of which 186 were upregulated and 156 were downregulated.Among them,the expression of SQLE was significantly higher in lung squamous cell carcinoma than in adjacent tissues.Comparison of Oncomine software showed that the expression of SQLE in lung squamous cell carcinoma was significantly higher than that in lung adenocarcinoma,small cell lung cancer,and benign lung;the expression level of SQLE in lung squamous cell carcinoma was significantly higher than that in paracancer tissue,p< 0.05,the difference was statistically significant.Kaplan-Meier survival curve analysis showed that the higher the expression of SQLE in patients with squamous cell carcinoma,the shorter the survival time,P<0.05,the difference was statistically significant.Therefore,we are expected to use SQLE as one of the biomarkers for early diagnosis and prognosis.The proliferation of NCI-H520 cell line after down-regulating SQLE in si-SQLE 1640 group was significantly lower than that in the normal group(p<0.001,the difference was statistically significant).The expression of p-ERK1/2 in the down-regulated group was significantly lower than that in the normal group.Analysis conclusion1.The high expression of SQLE in lung squamous cell carcinoma is one of the factors of poor prognosis.2.SQKE can promote cancer cell proliferation through its effect on the ERK pathway.