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Lung cancer is the leading cause of cancer death in men and the second leading cause of cancer death in women worldwide. Fascin-1 and laminin-5 were associated with the invasiveness and prognoses of several cancers. The expression and the serum levels of fascin-1 and laminin-5 in patients with non-small cell lung cancer (NSCLC) were analyzed in this study. The expression of fascin-1 and laminin-5 were examined in 378 patients and their serum level was measured in 154 patients. The health of all patients was followed post-surgery. The expression of fascin-1 (P = 0.000) and lanminin-5 (P = 0.001) and the serum levels of fascin-1 (P = 0.015) and laminin-5 (P = 0.046) were related to the relapse of patients with NSCLC. Both serum levels and expression of fascin-1 and laminin-5 can be used to effectively evaluate the prognoses of patients with NSCLC.

Ulcerative colitis (UC) is an immune-related disease with genetic predisposition. The aim of this study was to investigate the association of three polymorphisms in the receptor for advanced glycation end-products (RAGE) gene with UC risk in a Chinese population. This case-control study involved 72 UC patients and 479 age- and gender-matched healthy controls. Genotyping was performed using the polymerase chain reaction-ligase detection reaction method. Data were analyzed using the Haplo.stats program. There were no significant differences between patients and controls in the allele/genotype distributions of rs1800624 (P(allele)= 0.11; Pgenotype = 0.20), rs1800625 (P(allele) = 0.16; Pgenotype = 0.11), or rs2070600 (P(allele) = 0.37; Pgenotype = 0.65). In addition, no positive haplotypes were identified. To the best of our knowledge, the current study describes polymorphisms of RAGE in Chinese UC for the first time. We found no association between RAGE polymorphisms and the development of UC in the Chinese population.

The association between the human 8-oxoguanine glycosylase 1 (hOGG1) gene Ser326Cys polymorphism (rs1052133) and gastric cancer has been widely evaluated, yet a definitive answer to whether this association exists is lacking. We first conducted a case-control study to assess this association in a large Han Chinese population, and then performed a meta-analysis to further address this issue. This case-control study involved 448 patients clinically diagnosed with gastric cancer and 372 cancer-free control individuals from China. Genotyping was conducted using the polymerase chain reaction-ligase detection reaction method. Meta-analysis was performed by the STATA software. Data and study quality were assessed in duplicate. Our case-control association study indicated that there were no significant differences in the genotype and allele distributions of the Ser326Cys polymorphism between gastric cancer patients and controls (P = 0.8026 for genotype, and P = 0.5857 for allele), consistent with the results of the subsequent meta-analysis involving 2745 patients and 4588 controls under both allelic [odds ratio (OR) = 1.02; 95% confidence interval (CI) = 0.91-1.14; P = 0.739] and dominant (OR = 0.97; 95%CI = 0.78-1.21; P = 0.803) models. Further subgroup analyses by ethnicity, source of controls, and sample size also did not detect any positive associations in this meta-analysis. Overall, our study in the Han Chinese population, along with the meta-analysis, failed to confirm the association of the hOGG1 gene Ser326Cys polymorphism with gastric cancer risk, even across different ethnic populations.

Propofol is one of the extensively and commonly used intravenous anesthetic agents. The current study aimed to evaluate the effects of propofol on the behavior of human gastric cancer cells and the molecular mechanisms of this activity. The effects of propofol on SGC7901 and AGS cell proliferation, apoptosis, and invasion were detected by MTT assay, flow cytometric analysis, and matrigel invasion assay. Real-time polymerase chain reaction (PCR) was used to assess microRNA (miR)-221 expression. miR-221 mimics were transfected into SGC7901 and AGS cells to assess the role of miR- 221 in propofol-induced anti-tumor activity. Propofol significantly inhibited cell proliferation and invasion and promoted apoptosis of SGC7901 and AGS cells. Propofol also efficiently reduced miR-221 expression. Moreover, transfection of miR-221 mimics reversed the effects of propofol on the biological behavior of gastric cancer cells. Propofol can effectively inhibit proliferation and invasion and induce apoptosis of gastric cancer cells through, at least partly, downregulation of miR-221 expression.

Propofol is a commonly used intravenous anesthetic. We evaluated its effects on the behavior of human pancreatic cancer cells and the underlying molecular mechanisms. The effects of propofol on Panc-1 cell proliferation, apoptosis, and invasion were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, caspase-3 activity measurement, and Matrigel invasion assay. Quantitative polymerase chain reaction (qPCR) was used to assess microRNA-133a (miR-133a) expression. Anti-miR-133a was transfected into Panc-1 cells to assess the role of miR-133a in propofol-induced antitumor activity. Propofol significantly inhibited Panc-1 cell proliferation and invasion, and promoted apoptosis. Propofol also efficiently elevated miR-133a expression. Moreover, transfection of anti-miR-133a reversed the effects of propofol on the biological behavior of Panc-1 cells. Propofol can effectively inhibit proliferation and invasion, and induce apoptosis of pancreatic cancer cells, at least partly through the upregulation of miR-133a expression.

Lung cancer is a common malignant tumor worldwide and is now the leading cause of cancer-related deaths. Monocyte chemoattractant protein 1 (MCP-1) and its receptor chemokine receptor 2 (CCR-2) are important chemokines. We examined the polymorphisms of 338 unrelated patients with non-small cell lung carcinoma (NSCLC) and 200 unrelated healthy controls of Han nationality in Northern China using polymerase chain reaction-restriction fragment length polymorphism. We found a significant increase in the frequency of the MCP-1 AA genotype [0.293 vs 0.195, odds ratio (OR) = 1.71, 95% confidence interval (CI) = 1.13-2.60] and a significant decrease in the frequency of the GG genotype (0.290 vs 0.41, OR = 0.64, 95%CI = 0.47-0.87) in NSCLC patients compared to controls. The frequencies of AA-ww (0.151 vs 0.090, P = 0.041, OR = 1.80, 95%CI = 1.33-2.43) and AA-wm (0.136 vs 0.080, P = 0.049, OR = 1.81, 95%CI = 1.01-3.27) were higher in lung cancer patients than in healthy controls; the frequency of GG-wm (0.121 vs 0.190, P = 0.030, OR = 0.60, 95%CI = 0.38-0.95) was lower in lung cancer patients than in healthy controls. Based on these results, the polymorphism in MCP-1 may be correlated with the development of NSCLC in the Han nationality of Northern China. However, the polymorphism in CCR-2 is not involved in NSCLC.

Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues that form the pancreas. To investigate whether the tribbles homolog 1 (Drosophila) gene (TRIB1) is associated with pancreatic cancer in the Chinese Han population, we conducted this case-control study and genotyped 3 single nucleotide polymorphisms (rs2980879, rs2980874, and rs2235108) of the TRIB1 gene in 182 patients and 359 normal controls of Chinese Han origin and analyzed their association. The results showed that the rs2980879 polymorphism was associated with pancreatic cancer [allele: P = 0.023434, genotype: P = 0.03005; odds ratio (OR) and 95% confidence interval (CI) = 0.727788 (0.552664-0.958404)], whereas the rs2980874 polymorphism had no association with pancreatic cancer [allele: P = 0.749885, genotype: P = 0.699533; OR and 95%CI = 1.041981 (0.809196-1.341734)], and the rs2235108 polymorphism was not associated with the disease [allele: P = 0.629475, genotype: P = 0.547534, OR and 95%CI = 1.128290 (0.690829-1.842770)]. Haplotype analyses and linkage disequilibrium tests were also conducted, and the results showed that these 3 loci are not in the same block. In conclusion, our study indicated that the TRIB1 gene is associated with pancreatic cancer. More studies with larger samples are needed in order to support this finding.

The gene encoding vitamin D receptor (VDR) is recognized as a promising candidate for indicating the development of inflammatory bowel disease (IBD). Four genetic polymorphisms (ApaI, BsmI, FokI, TaqI) in VDR have been widely evaluated to determine their association with IBD, and the results of these evaluations are often inconsistent. Therefore, we conducted a meta-analysis to shed some light on this issue and explored the sources of the heterogeneity between studies. We identified six articles for ApaI (cases/controls: 1902/1468), eight for TaqI (3053/2145), and five each for BsmI (1512/1616) and FokI (2315/1676). Data were analyzed under the random-effects model, and heterogeneity was explored by subgroup analyses. Overall, except for TaqI in allelic comparison [odds ratio (OR) = 0.90, 95% confidence interval (CI): 0.83-0.98], ApaI, BsmI, and FokI polymorphisms showed no significant associations with IBD across different genetic models of inheritance. However, subgroup analyses indicated significance for the association of ApaI with Crohn's disease (CD) risk (AA versus aa: OR = 1.40; 95%CI = 1.05-1.88), for BsmI in East Asians (BB plus Bb versus bb: OR = 1.77, 95%CI = 1.14-2.74), for TaqI in Caucasians (TT plus Tt versus tt: OR = 0.79, 95%CI = 0.63- 1.00), and with ulcerative colitis (UC) risk (T versus t: OR = 0.89, 95%CI = 0.80-0.99). There was a low probability of publication bias for all studied polymorphisms. Pooling previous individual studies on IBD, our findings demonstrated that the ApaI polymorphism may increase the risk of CD, whereas the TaqI polymorphism may decrease the risk of UC, especially in Caucasians. Moreover, this study leaves open the question of divergent genetic profiles across different ethnic groups.

Ulcerative colitis (UC) is a chronic inflammation of the large intestine. The aim of this study was to investigate the association of two polymorphisms in STAT3 with the risk of UC development in the Chinese Han population. This is a hospital-based case-control study involving 56 UC patients and 274 controls. Genotyping was performed using the polymerase chain reaction with sequence-specific primers (PCR-SSP) method. Statistical analyses were conducted using logistic regression and genotype risk score. Overall, there was a significant difference between patients and controls in the genotype distribution of rs2293152 (P = 0.044). The risk for UC associated with the rs2293152-G mutant allele was increased (odds ratio = 2.76; 95% confidence interval = 1.06- 7.24) under the dominant model. However, we failed to find any obvious differences in the rs4796793 genotype or allele distributions between the UC patients and controls, and did not detect any significant association of the rs4796793 polymorphism with UC across different genetic models of inheritance. Our study implies that the STAT3 rs2293152 polymorphism may be associated with the occurrence of UC and might be used as a predictive factor for UC in the Chinese Han population.

Epoxide hydrolases metabolize exogenous chemicals, including carcinogens such as polycyclic aromatic hydrocarbons. The relationship between microsomal epoxide hydrolase 1 (EPHX1) polymorphisms and esophageal cancer risk has been investigated in various ethnic populations, but the results have been contradictory. We investigated the association of EPHX1 Tyr113His and His139Arg polymorphisms with esophageal cancer via a comprehensive meta-analysis. Publications before August 20, 2012 were included. Eight studies concerning Tyr113His polymorphism associated with 1158 esophageal cancer cases and 1868 controls were identified; 7 studies concerning association of His139Arg with 901 esophageal cancer cases and 1615 controls were also included. A random-effect model was applied, irrespective of between-study heterogeneity. Data and study quality were assessed in duplicate. No significant association was found in either the allele or genotype models for Tyr113His or His139Arg polymorphism with risk for esophageal cancer. Lack of association was also identified in stratified analyses by ethnicity. No publication bias was observed. We conclude that current evidence does not demonstrate association of EPHX1 Tyr113His or His139Arg polymorphisms with risk for development of esophageal cancer.

Interleukin 6 (IL6) is a pleiotropic cytokine involved in physiological processes and in a variety of human malignancies. It is thus a logical candidate for being a causative factor underlying colorectal cancer (CRC). The association between the IL6 -174G>C polymorphism and CRC has been widely evaluated; yet, there is a lack of agreement between studies on the role of this polymorphism in CRC. We performed a meta-analysis to evaluate this association signal. Articles published before May 10, 2012 were included in the meta-analysis. A total of 11 populations incorporating 6481 cases and 7935 controls were included in our analysis. A random-effect model was applied irrespective of between-study heterogeneity. Data and study quality were assessed in duplicate. Overall, the association of the -174G>C polymorphism with CRC was not significant in an allelic comparison model [odds ratio (OR) = 0.99; 95% confidence interval (95%CI) = 0.90-1.09; P = 0.827], a homozygote model (OR = 0.98; 95%CI = 0.83-1.15; P = 0.805), a dominant model (OR = 0.99; 95%CI = 0.87-1.13; P = 0.906), or a recessive model (OR = 0.97; 95%CI = 0.88-1.08; P = 0.610). Furthermore, the analyses of subgroups created based on common study design, genotyping methods, and ethnicity failed to find a significant association of this polymorphism with CRC. Therefore, our results collectively suggest that the IL6 -174G>C polymorphism might not be a potential candidate for CRC risk.

The association between the Cyclin D1 gene (CCND1) G870A polymorphism and esophageal cancer has been widely evaluated, with conflicting results. As meta-analysis is a reliable approach to resolving discrepancies, we aimed to evaluate this association. Data were available from 9 study populations incorporating 1898 cases and 3046 controls. Overall, the allelic/genotypic association between the G870A polymorphism and esophageal cancer was nonsignificant [for allele: odds ratio (OR) = 1.14, 95% confidence interval (95%CI) = 0.94-1.38, P = 0.184; for genotype homozygous comparison: OR = 1.36, 95%CI = 0.90-2.06, P = 0.140; for dominant model: OR = 1.24, 95%CI = 0.88-1.75, P = 0.222; for recessive model: OR = 1.13, 95%CI = 0.90-1.43, P = 0.292]. Moreover, subgroup analyses according to study designs, geographic areas, types of esophageal cancer, genotyping methods, and ethnicities failed to demonstrate a significant association between this polymorphism and esophageal cancer. In addition, there was significant publication bias as reflected by funnel plots and the Egger test (P = 0.042). Taken together, our results suggest that the CCND1 G870A polymorphism might not be a potential candidate for predicting esophageal cancer risk.

The association between the NAD(P)H: quinone oxidoreductase 1 (NQO1) gene C609T polymorphism and gastric cancer has been widely evaluated, yet with conflicting results. Data were available from seven study populations involving 2600 subjects. Overall, comparison of alleles 609T and 609C indicated a significantly increased risk (46%) for gastric cancer (95% confidence interval (95%CI) for odds ratio (OR) = 1.20-1.79) in individuals with the T allele. The tendency was increased in the homozygous comparison (609TT versus 609CC), with an OR = 2.04 (95%CI = 1.37-3.05). Stratified analysis by study design demonstrated stronger associations in population-based studies than in hospital-based studies, based on OR. Ethnicity-based analysis demonstrated a significant association in Asians but not in Caucasians. Additionally, in the subgroup analyses by the type of gastric cancer, a significantly increased risk was found with all genetic models in the gastric adenocarcinoma subgroup compared to the others. We conclude that the NQO1 gene C609T polymorphism increases the risk for gastric cancer, especially in Asian populations.