Objective:To explore the role and mechanism of serum response factor (SRF) and lncRNA FGD5-AS1 in lung adenocarcinoma (LUAD).Methods:The plasma and tissue wax of LUAD patients treated in Tangshan People's Hospital from 2020 to 2022 and the plasma of healthy people were collected. The expression of SRF in LUAD tissues and cells, and the expression of lncRNA FGD5-AS1 in LUAD tissues, plasma and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of SRF and lncRNA FGD5-AS1 in LUAD tissue microarray were detected by immunohistochemistry and in situ hybridization. LUAD cells A549, H1299 and H1975 were cultured in vitro and divided into si-NC and si-SRF groups, si-NC and si-lncRNA FGD5-AS1 groups, pcDNA3.1 and lncRNA FGD5-AS1 groups, si-NC+pcDNA3.1/si-SRF+pcDNA3.1/si-SRF+lncRNA FGD5-AS1 groups. The effects of the above groups on the proliferation, invasion and migration of LUAD cells were detected by CCK-8, cloning formation, EdU, Transwell and scratch test. The JASPAR database was used to predict the downstream lncRNA FGD5-AS1 that can be regulated by SRF; double luciferase experiment, chromatin Immunoprecipitation (CHIP) and electrophoretic mobility shift assay (EMSA) experiment were used to verify the regulatory effect between SRF and lncRNA FGD5-AS1, and the subcutaneous tumorigenesis experiment in nude mice was used to detect the effects of cells that stably knock down SRF and stably overexpress lncRNA FGD5-AS1 on the growth of transplanted tumors. Results:The results of immunohistochemistry showed that the mean optical density of SRF in LUAD tissues (1.49±0.33) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The expression level of SRF in paraffin tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.037). CCK-8, cloning, scratch and Transwell experiments showed that knockdown SRF could inhibit the proliferation, migration and invasion of A549 and H1299 cells, respectively. [For A549 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (233.70±18.50), (808.70±6.11), (489.70±53.00), and 1.00±0.03, respectively, in the si-NC group; and (131.30±22.50), (403.00±9.54), (372.70±26.27), and 2.14±0.09, respectively, in the si-SRF group. For H1299 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (194.30±20.98), (988.70±64.52), (907.70±67.02), and 1.00±0.05, respectively, in the si-NC group; and (137.70±7.77), (665.70±157.10), (565.70±67.01), and 1.52±0.03, respectively, in the si-SRF group. All comparisons showed statistically significant differences ( P＜0.05)] JASPAR database prediction shows that SRF and lncRNA FGD5-AS1 have binding site. The double luciferase experiment, CHIP and EMSA experiments showed that SRF could regulate lncRNA FGD5-AS1. In situ hybridization showed that the mean optical density of lncRNA FGD5-AS1 in tissue microarray of LUAD patients (1.28±0.31) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The results of qRT-PCR experiment showed that the expression level of lncRNA FGD5-AS1 in wax tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.017). The expression level of lncRNA FGD5-AS1 in plasma of LUAD patients (3.48±2.62) was higher than that of healthy people (1.02±0.03, P＜0.001). CCK-8, cloning, EDU, scratch and Transwell experiments showed that overexpression of lncRNA FGD5-AS1 could promote cell proliferation [For A549 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (22.67±5.86), (1.00±0.09), (135.70±13.20), and 0.35±0.02, respectively, in the pcDNA3.1 group; and (46.33±9.07), (1.65±0.10), (205.00±13.23), and 0.20±0.01, respectively, in the FGD5-AS1-overexpressing group. All comparisons showed statistically significant differences ( P＜0.05)], migration and invasion and vice versa [For H1975 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (75.33±4.16), (1.00±0.02), (258.70±45.79), and 0.18±0.01, respectively, in the NC group; and (37.00±4.00), (0.52±0.07), (130.70±9.07), and 0.53±0.04, respectively, in the lncRNA FGD5-AS1 knockdown group (si-lncRNA FGD5-AS1 group). All comparisons showed statistically significant differences ( P＜0.05)]. Overexpression of lncRNA FGD5-AS1 could rescue the effect of knockdown SRF on the proliferation, migration and invasion of A549 and H1299 cells. The results of subcutaneous tumorigenesis experiment in nude mice indicated that the tumorigenicity of LUAD cells stably knockdown SRF was weakened and vice versa. Conclusion:SRF can promote the progress of LUAD by regulating lncRNA FGD5-AS1.

Objective:To explore the role and mechanism of serum response factor (SRF) and lncRNA FGD5-AS1 in lung adenocarcinoma (LUAD).Methods:The plasma and tissue wax of LUAD patients treated in Tangshan People's Hospital from 2020 to 2022 and the plasma of healthy people were collected. The expression of SRF in LUAD tissues and cells, and the expression of lncRNA FGD5-AS1 in LUAD tissues, plasma and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of SRF and lncRNA FGD5-AS1 in LUAD tissue microarray were detected by immunohistochemistry and in situ hybridization. LUAD cells A549, H1299 and H1975 were cultured in vitro and divided into si-NC and si-SRF groups, si-NC and si-lncRNA FGD5-AS1 groups, pcDNA3.1 and lncRNA FGD5-AS1 groups, si-NC+pcDNA3.1/si-SRF+pcDNA3.1/si-SRF+lncRNA FGD5-AS1 groups. The effects of the above groups on the proliferation, invasion and migration of LUAD cells were detected by CCK-8, cloning formation, EdU, Transwell and scratch test. The JASPAR database was used to predict the downstream lncRNA FGD5-AS1 that can be regulated by SRF; double luciferase experiment, chromatin Immunoprecipitation (CHIP) and electrophoretic mobility shift assay (EMSA) experiment were used to verify the regulatory effect between SRF and lncRNA FGD5-AS1, and the subcutaneous tumorigenesis experiment in nude mice was used to detect the effects of cells that stably knock down SRF and stably overexpress lncRNA FGD5-AS1 on the growth of transplanted tumors. Results:The results of immunohistochemistry showed that the mean optical density of SRF in LUAD tissues (1.49±0.33) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The expression level of SRF in paraffin tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.037). CCK-8, cloning, scratch and Transwell experiments showed that knockdown SRF could inhibit the proliferation, migration and invasion of A549 and H1299 cells, respectively. [For A549 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (233.70±18.50), (808.70±6.11), (489.70±53.00), and 1.00±0.03, respectively, in the si-NC group; and (131.30±22.50), (403.00±9.54), (372.70±26.27), and 2.14±0.09, respectively, in the si-SRF group. For H1299 cells: The clone formation count, migration count, invasion count, and 48-h migration distance ratio were (194.30±20.98), (988.70±64.52), (907.70±67.02), and 1.00±0.05, respectively, in the si-NC group; and (137.70±7.77), (665.70±157.10), (565.70±67.01), and 1.52±0.03, respectively, in the si-SRF group. All comparisons showed statistically significant differences ( P＜0.05)] JASPAR database prediction shows that SRF and lncRNA FGD5-AS1 have binding site. The double luciferase experiment, CHIP and EMSA experiments showed that SRF could regulate lncRNA FGD5-AS1. In situ hybridization showed that the mean optical density of lncRNA FGD5-AS1 in tissue microarray of LUAD patients (1.28±0.31) was higher than that in adjacent tissues (1.00±0.00, P＜0.001). The results of qRT-PCR experiment showed that the expression level of lncRNA FGD5-AS1 in wax tissues of LUAD patients was higher than that in normal tissues adjacent to cancer ( P=0.017). The expression level of lncRNA FGD5-AS1 in plasma of LUAD patients (3.48±2.62) was higher than that of healthy people (1.02±0.03, P＜0.001). CCK-8, cloning, EDU, scratch and Transwell experiments showed that overexpression of lncRNA FGD5-AS1 could promote cell proliferation [For A549 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (22.67±5.86), (1.00±0.09), (135.70±13.20), and 0.35±0.02, respectively, in the pcDNA3.1 group; and (46.33±9.07), (1.65±0.10), (205.00±13.23), and 0.20±0.01, respectively, in the FGD5-AS1-overexpressing group. All comparisons showed statistically significant differences ( P＜0.05)], migration and invasion and vice versa [For H1975 cells: The clone formation count, EdU-positive cell count, invasion count, and 48-h migration distance ratio were (75.33±4.16), (1.00±0.02), (258.70±45.79), and 0.18±0.01, respectively, in the NC group; and (37.00±4.00), (0.52±0.07), (130.70±9.07), and 0.53±0.04, respectively, in the lncRNA FGD5-AS1 knockdown group (si-lncRNA FGD5-AS1 group). All comparisons showed statistically significant differences ( P＜0.05)]. Overexpression of lncRNA FGD5-AS1 could rescue the effect of knockdown SRF on the proliferation, migration and invasion of A549 and H1299 cells. The results of subcutaneous tumorigenesis experiment in nude mice indicated that the tumorigenicity of LUAD cells stably knockdown SRF was weakened and vice versa. Conclusion:SRF can promote the progress of LUAD by regulating lncRNA FGD5-AS1.

Objective To study expression and prognostic value of Shugoshin-1(SGOL1)in lung adenocarcinoma by bioinformatics method.Methods Expression profile data and clinical data of lung adenocarcinoma and normal tissues were downloaded from The Cancer Genome Atlas database,and expression difference and clinical correlation analysis of SGOL1 were performed.R package"pROC"was used to plot receiver operator characteristic(ROC)curves to evaluate accuracy of SGOL1 expression in predicting clinical diagnosis in lung adenocarcinoma patients.Effects of SGOL1 expression on prognosis of lung adenocarcinoma patients were evaluated by R package"survival","survminer"and univariate and multivariate Cox regression analysis.By searching Tumor Immune Single-Cell Hub and TIMER2.0 databases,expression distribution of SGOL1 in lung adenocarcinoma and its relationship with immune cell infiltration were analyzed,functional enrichment analysis of SGOL1 and its co-expression was performed by using LinkedOmics database.Search tool for the retrieval of interaction gene/proteins was used to construct a protein-protein interaction network for SGOL1.Results Compared with normal tissues,expression level of SGOL1 in tumor tissues was significantly upregulated(P<0.001).Compared with paracancer tissues,expression level of SGOL1 in tumor tissues was significantly upregulated(P<0.001).In different clinical and pathological stages of lung adenocarcinoma,compared with stage Ⅰ,expression levels of SGOL1 in stages Ⅱ,Ⅲ and Ⅳ were significantly higher(P<0.05).ROC curve showed that SGOL1 had a good diagnostic efficiency in lung adenocarcinom patients,with area under the curve of 0.959(95%CI:0.942-0.975).Overall survival,disease specific survival,disease-free survival and progression free interval of high expression group of SGOL1 were significantly shorter than those of low expression group of SGOL1(P<0.05).Univariate and multivariate Cox regression analysis showed that clinical stage(HR=1.629,P<0.001)and SGOL1 expression level(HR=1.447,P=0.002)were associated with poor prognosis in lung adenocarcinoma patients.It can be used as an independent risk factor for the prognosis of lung adenocarcinoma patients.Expression level of SGOL1 was negatively correlated with infiltration level of B cells,CD4+T cells and dendritic cells(P<0.05).Expression level of SGOL1 was positively correlated with infiltration level of macrophages,CD8+T cells and neutrophils(P<0.05).Enrichment analysis showed that SGOL1 may play role in mitosis,cell cycle,p53 signaling pathway and amino acid metabolism pathways.Analysis of protein-protein interaction network suggests that SGOL1 was closely related to multiple molecules such as CBX1,PPP2CA,PPP2R5C,CDCA8,ESPL1,PPP2R1A,BUB1,PPP2R5A,SGO2,CDC20,etc.Conclusion SGOL1 is highly expressed in lung adenocarcinoma tissues,and it is associated with poorer prognosis in lung adenocarcinoma patients.SGOL1 can be used as one of prognostic biomarkers for lung adenocarcinoma patients.

Purpose/Significance To analyze the multidimensional interaction between the characteristics of traditional Chinese and western medicine in patients with type 2 diabetes mellitus and its influence on traditional Chinese medicine(TCM)syndrome differentia-tion.Method/Process Based on the real-world electronic medical record(EMR)data,the traditional association rule algorithm is im-proved,and the important TCM syndromes are screened out as dependent variables by increasing the respect index,and the logistic regres-sion algorithm is used to explore the influence of traditional Chinese and western medicine indexes on TCM syndromes.Result/Conclusion Based on 688 patients,112 association rules are obtained,of which 12 includes TCM syndromes.The respect of association rules between middle-earth stagnation syndrome and overweight/obesity is the highest,moreover,overweight/obesity patients have a higher prevalence rate of middle-earth stagnation syndrome.There is a strong correlation between middle-earth stagnation syndrome,peripheral neuropathy or hypertension and overweight/obesity.Patients with diabetic nephropathy are more likely to have qi and yin deficiency syndrome.

Nonalcoholic fatty liver disease (NAFLD), especially nonalcoholic steatohepatitis (NASH), is a common hepatic manifestation of metabolic syndrome. However, there are no effective therapy to treat this devastating disease. Accumulating evidence suggests that the generation of elastin-derived peptides (EDPs) and the inhibition of adiponectin receptors (AdipoR)1/2 plays essential roles in hepatic lipid metabolism and liver fibrosis. We recently reported that the AdipoR1/2 dual agonist JT003 significantly degraded the extracellular matrix (ECM) and ameliorated liver fibrosis. However, the degradation of the ECM lead to the generation of EDPs, which could further alter liver homeostasis negatively. Thus, in this study, we successfully combined AdipoR1/2 agonist JT003 with V14, which acted as an inhibitor of EDPs-EBP interaction to overcome the defect of ECM degradation. We found that combination of JT003 and V14 possessed excellent synergistic benefits on ameliorating NASH and liver fibrosis than either alone since they compensate the shortage of each other. These effects are induced by the enhancement of the mitochondrial antioxidant capacity, mitophagy, and mitochondrial biogenesis via AMPK pathway. Furthermore, specific suppression of AMPK could block the effects of the combination of JT003 and V14 on reduced oxidative stress, increased mitophagy and mitochondrial biogenesis. These positive results suggested that this administration of combination of AdipoR1/2 dual agonist and inhibitor of EDPs-EBP interaction can be recommended alternatively for an effective and promising therapeutic strategy for the treatment of NAFLD and NASH related fibrosis.

Objective The expression and prognosis significance of CD59 in pancreatic cancer were analyzed by bioinformatics.Methods Gene expression profiling interactive analysis 2(GEPIA2)and human protein atlas(HPA)databases were used to compare the expression of CD59 between pancreatic cancer tissues and adjacent tissues;Kaplan-Meier plotter database was used to evaluate the effect of CD59 on prognosis;String and Cytoscape3.9.1 were used to analyze the CD59 protein interaction network;DAVID6.8 performed gene enrichment and pathway enrichment analysis of CD59 with key interacting genes.Results Compared with normal tissues,the expression of CD59 in pancreatic cancer tissues was significantly up-regulated(P<0.05),and the overall survival time(HR=2.3,95%CI:1.52-3.50)and recurrence free survival(HR=4.31,95%CI:1.57-11.83)of pancreatic cancer patients with CD59 high expression was shorter than CD59 low expression patients.Protein interaction network analysis revealed that CD59 is closely related to several molecules such as CD55,GOLGA2,LMAN1,TMED2 and SERPINA1.Gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis indicated that CD59 was mainly involved in pathways such as complement activation,innate immune response and coronavirus-COVID-19.Conclusion CD59 is highly expressed in pancreatic cancer tissue and is affected by several immune-related genes.It is associated with poor prognosis of patients and can be used as one of biomarkers for early diagnosis and prognosis prediction of pancreatic cancer.

Currently, there is still no effective curative treatment for the development of late-stage liver fibrosis. Here, we have illustrated that TB001, a dual glucagon-like peptide-1 receptor/glucagon receptor (GLP-1R/GCGR) agonist with higher affinity towards GCGR, could retard the progression of liver fibrosis in various rodent models, with remarkable potency, selectivity, extended half-life and low toxicity. Four types of liver fibrosis animal models which were induced by CCl₄, α-naphthyl-isothiocyanate (ANIT), bile duct ligation (BDL) and Schistosoma japonicum were used in our study. We found that TB001 treatment dose-dependently significantly attenuated liver injury and collagen accumulation in these animal models. In addition to decreased levels of extracellular matrix (ECM) accumulation during hepatic injury, activation of hepatic stellate cells was also inhibited via suppression of TGF-β expression as well as downstream Smad signaling pathways particularly in CCl₄-and S. japonicum-induced liver fibrosis. Moreover, TB001 attenuated liver fibrosis through blocking downstream activation of pro-inflammatory nuclear factor kappa B/NF-kappa-B inhibitor alpha (NFκB/IKBα) pathways as well as c-Jun N-terminal kinase (JNK)-dependent induction of hepatocyte apoptosis. Furthermore, GLP-1R and/or GCGR knock-down results represented GCGR played an important role in ameliorating CCl₄-induced hepatic fibrosis. Therefore, TB001 can be used as a promising therapeutic candidate for the treatment of multiple causes of hepatic fibrosis demonstrated by our extensive pre-clinical evaluation of TB001.

Objective:To investigate the effect of different chemotherapy drugs combined with DNA methylase inhibitor 5-Aza-2'-deoxycytidine (5-Aza-dC) on the apoptosis of lung adenocarcinoma cells.Methods:In the prospective randomized controlled study, lung adenocarcinoma A549 cells were treated with cisplatin plus paclitaxel (TP) or gemcitabine (GP) with or without 5-Aza-dC. According to different drug intervention methods, they were divided into control group, cisplatin combined with paclitaxel (TP) group, cisplatin combined with gemcitabine (GP) group, and 5-Aza-dC combined with TP group, 5-Aza-dC combined with GP group. CCK-8 assay was used to detect the proliferation of A549 cells. Transwell migration and invasion assay were used to detect the effect that each group of drugs on the migration and invasion ability of A549 cells. Quantitative Real-time Polymerase Chain Reaction was used to evaluate the effect of each treatment on the expression of apoptotic genes. One-way analysis of variance was used to compare the degree of cell proliferation in different drug treatment groups, and LSD- t method was used for pairwise comparison within groups. Results:The inhibition rates of lung adenocarcinoma cells in the TP regimen at different time points at 24, 48, and 72 h were as follows (20.00±4.23) %, (35.00±2.80) %, and (56.00±3.11) %. The inhibition rate of 5-Aza-dC combined with TP regimen on lung adenocarcinoma cells was significantly increased, at different time points of 24, 48 and 72 h, respectively (38.00±3.80) %, (50.00±3.25) %, (93.00±4.33) %. The inhibition rates of cells at different time points at 24, 48, and 72 h in the GP regimen were (33.00±5.10) %, (54.00±3.80) %, and (74.00±2.82) %, respectively; while 5-Aza-dC combined with GP regimen could significantly reduce the rate of cell growth, the inhibition rates of cells at 24, 48, and 72 h different time points were as follows (54.00±3.00) %, (67.00±5.30) %, and (95.00±1.13) %. The inhibitory effect of the same drug on lung adenocarcinoma cells increased with time (TP group: F=35.93, P<0.001; 5-Aza-dC combined with TP group: F=97.33, P<0.001; GP group: F =41.73, P<0.001; 5-Aza-dC combined with GP group: F=79.00, P<0.001), and at different time points, the differences were statistically different (all P<0.05). 5-Aza-dC combined with TP and GP chemotherapy regimens can inhibit the migration and invasion of lung adenocarcinoma cell A549, and the inhibitory effect is stronger than that of TP or GP regimens alone. The expression of Caspase 8 was significantly elevated ( t=5.87, P=0.004) in cells treated with 5-Aza-dC combined with GP when compared with GP regimen alone. The expression of Caspase 8 ( t=3.94, P=0.017), Caspase 6 ( t=5.81, P=0.004) and BBC3 (BCL-2 binding component 3) ( t=6.53, P=0.003) were increased when drugged with 5-Aza-dC combined TP regimen compared with TP regimen alone. Conclusion:5-Aza-dC might serve as a chemotherapeutic sensitizer to increase the sensitivity of lung adenocarcinoma cells.

Objective:To observe the efficacy and safety of oral administration of low-molecular-weight collagen peptide on facial skin rejuvenation.Methods:A total of 66 female volunteers in Department of Dermatology, Beijing Friendship Hospital, Capital Medical University aged from 35 to 50 years old (average 42.89±4.44) from November 2018 to February 2019 were enrolled and randomly divided into two groups, 33 cases each. The testing group was given 5 g Su Yan Xin Ji collagen peptide for 12 weeks; the control group was given 5 g Tai Duo Jian collagen protein powder for 12 weeks. The effects were evaluated and analyzed using VISIA and CK complexion analysis system before and after 1, 2, 4 , 12 weeks of oral administration collagen; meanwhile, the volunteers' overall satisfaction and adverse reactions were also recorded.Results:In total, 61 volunteers completed the study. After 12 weeks of oral administration, the skin hydration of testing group and control group were all increased (65.41±10.60 vs 59.82±9.26), the transepidermal water loss, wrinkles, textures, pores, red areas and porphyrin were all decreased (19.19±4.24 vs.21.50±5.10; 7.38±3.67 vs. 8.98±6.67; 5.55±3.07 vs.6.60±4.84; 16.94±9.30 vs. 17.95±8.85; 21.92±4.60 vs. 22.11±5.34; 10.31±7.03 vs. 11.62±8.58). There were statistically significant differences between the 7 parameters before and after oral administration ( P<0.05). The difference of skin hydration between the testing and control group was statistically significant ( t=2.317, P=0.024). Although there was no statistical difference among the other six parameters, the improvement degree of the testing group was better than that of the control group. Surface spots, UV spots and brown spots of two groups showed no significant difference before and after treatment. Overall satisfaction of the testing group and the control group were 86.67% vs. 61.29% with significant difference 12 weeks after treatment ( χ2=5.074, P=0.024), while there were no significant differences in incidence of adverse reactions between two groups ( P>0.05). Conclusions:Oral administration of low-molecular-weight-collagen peptide can improve skin textures, moisturize skin with high overall satisfaction. It is an effective method of facial rejuvenation and better than that of collagen protein powder.

Objective: This study aimed to investigate the relationship between the genetic variation of CD55 promoter and the risk of esophageal cancer. Methods: A total of 700 esophageal cancer patients recruited between April 2008 and December 2012 at Tangshan Grongren Hospital and Tangshan Renmin Hospital, and 700 frequency matched controls were randomly selected from a pool of cancer free subjects recruited from a nutritional survey. Genotypes of CD55 rs2564978 polymorphism among all subjects were conducted by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The OR and 95%CI were calculated by non-conditional Logistic regression to evaluate the association of CD55 rs2564978T/C polymorphism with the risk of esophageal cancer. Results: The average age of cases and control was (60.04±9.19) and (59.21±9.98) years old. Compared with CD55 rs2564978 TT carriers, the individuals with CC genotype had a significantly higher risk of esophageal cancer (OR=1.94, 95%CI:1.42-2.66) . When stratified by sex, this genetic variation affected the risk of esophageal cancer among both males (OR=1.92, 95%CI:1.37-2.70) and females (OR=2.34, 95%CI:1.04-5.27). When stratified by age, the CD55 rs2564978 CC was associated with the susceptibility of developing esophageal cancer among younger individuals (OR=1.79, 95%CI:1.19-2.68) and older people (OR=2.32, 95%CI:1.41-3.83).When stratified by drinking status, CC genotype carriers increase the risk of esophageal cancer when drinking (OR=1.93, 95%CI:1.03-3.63) or not drinking (OR=1.95, 95%CI:1.36-2.80). When stratified by smoking status, CC genotype was associated with the risk of esophageal cancer among non-smokers (OR=1.79, 95%CI: 1.13-2.83), light smokers (less than 30 packs/year, OR=1.86, 95%CI:1.31-2.64) and heavy smokers (more than 30 packs/year, OR=2.67, 95%CI:1.28-5.57). Gene-environmental interaction analysis showed that CD55 rs2564978T/C polymorphism interacted with smoking status to increase the risk of esophageal cancer. Conclusion CD55 rs2564978 polymorphism effects on the risk of esophageal cancer.