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ABSTRACT: Invasion and metastasis are the most common causes of mortality for patients with colorectal neoplasms, and blocking invasion and metastasis in a timely fashion has become a hot research focus. We investigated the expression of the messenger RNA of Syndecan-1 and HPA-1 in colorectal cancer, and their correlation with invasion and metastasis.
Real-time fluorescent quantitative polymerase chain reaction (PCR) was used to detect the expression of Syndecan-1 and HPA-1 in specimens from 49 patients with colorectal cancer, 49 paired adjacent colorectal neoplasms (2 cm from the carcinoma), and 49 surgical margins of paired normal colorectal mucosa tissue (5 cm from the carcinoma), to analyze their correlation with clinicopathologic characteristics of colorectal neoplasm.
The expression of HPA-1 mRNA was significantly higher in colorectal cancer (40.56 +/- 11.75) than that in the paired adjacent colorectal neoplasms (18.28 +/- 11.33) and normal colorectal mucosa tissue (10.80 +/- 10.20) (all P < 0.001). The expression of HPA-1 mRNA was significantly higher in paired adjacent colorectal neoplasms than that in normal colorectal mucosa (P < 0.05). The expression of Syndecan-1 mRNA was significantly higher in normal colorectal mucosa (61.21 +/- 12.96) than in the paired adjacent mucosa (14.35 +/- 11.06) or colorectal cancer (10.12 +/- 8.58) (all P < 0.001). The expression of Syndecan-1 mRNA was significantly higher in the paired adjacent mucosa than that in colorectal cancer (P < 0.05). The decreased expression of Syndecan-1 mRNA and the increased expression of HPA-1 were closely associated with the degree of differentiation, the depth of infiltration, lymph node metastasis, vessel metastasis, and TNM staging of colorectal cancer (all P < 0.05). Spearman rank correlation analysis demonstrated a significant correlation between Syndecan-1 and HPA-1(r = -0.405, P < 0.05).
The expression of Syndecan-1 mRNA was significantly highest in normal colorectal mucosa and the expression of HPA-1 mRNA was significantly highest in colorectal cancer. At the same time, the decreased expression of Syndecan-1 mRNA and the increased expression of HPA-1 mRNA can promote the invasion and metastasis of colorectal cancer. The determination of Syndecan-1 and HPA-1 may be of value in the treatment as well as in the prognosis of patients with colorectal cancer.
Chinese journal of cancer 03/2010; 29(3):288-93.
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ABSTRACT: ObjectiveTo quantitatively explore the expression of Syndecan-1 and heparanase-1 in esophageal cancer tissue as well as their relationship
with the clinicopathological factors, in order to evaluate their roles in tumor invasion and metastasis.
MethodsReal-time fluorescence quantitative PCR (Q-PCR) was used to analyze the expression levels of Syndecan-1 and heparanase-1 genes,
participants included 67 cases with esophageal cancers and 32 healthy volunteers.
ResultsThe expression of Heparanase-1 gene in esophageal cancers was higher than that in normal esophageal tissue (P < 0.001), and the expression of Syndecan-1 gene in the normal esophageal tissue was higher compared with esophageal cancers
(P < 0.001). The positive rates of Syndecan-1 and Heparanase-1 gene in esophageal cancer were 13.4% (9/67) and 85.1% (57/67).
The expression of Syndecan-1 and Heparanase-1 genes was significantly related to diff erentiation, depth of infiltration,
lymph node metastasis, vessel metastasis, and TNM stages of disease (P < 0.05). In an attempt to measure the association between the 2 agents, this study found that the expression of Syndecan-1
mRNA had a significantly negative correlation with the expression of Heparanase-1 mRNA by using Spearman rank correlation
test (OR = −0.572, P < 0.001).
ConclusionSyndecan-1 and Heparanase-1 play important roles in the invasion and metastasis of esophageal cancer. The reduction of Syndecan-1
and/or the increase of Heparanase-1 may influence the invasion and metastasis of malignant tumors. Thus the combination assay
of Syndecan-1 and Heparanase-1 may contribute to the diagnosis and treatment of malignant tumors.
Key WordsSyndecan-1-esophageal neoplasms-neoplasm invasiveness-neoplasm metastasis-PCR
Clinical Oncology and Cancer Research 7(4):253-258.
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ABSTRACT: ObjectiveInterleukin-10 (IL-10) is a multifunctional cytokine with both immunosuppressive and antiangiogenic functions. Previous studies
have reported that IL-10 levels are significantly elevated in patients with gastric cancer (GC). It has also been confirmed
that interindividual variations in IL-10 production are genetically attributed to the polymorphisms of IL-10 gene. Therefore,
this study was designed to investigate whether the polymorphisms of IL-10 gene were associated with susceptibility to GC in
the Chinese population.
MethodsThe serum levels of IL-10 were measured by radioimmunoassay. The single nucleotide polymorphisms (SNPs) at positions −1082A/G,
−819T/C and −592A/C in the IL-10 gene promoter were analyzed using polymerase chain reaction-restriction fragment length polymorphism
Results220 patients with gastric cancer and 180 healthy controls were included in this study. The serum levels of IL-10 were significantly
higher in GC patients than healthy controls (Z = −19.13, P < 0.001). Single SNP analysis showed that the −1082G allele, −1082AG and −819CC genotypes significantly increased in patients
with GC (P = 0.029, 0.021, 0.039 respectively). In a logistic regression analysis adjusted for age and sex, the −1082AG genotype was
associated with an odds ratio of 1.974 (95% CI, 1.14–3.391; P = 0.014), and the −819CC genotype with an odds ratio of 2.496 (95% CI, 1.222–5.102; P = 0.012) for GC. Furthermore, haplotype analysis revealed that at least five haplotypes (ATA, ACC, GCC, ACA and ATC) were
existent in this population. Also that the GCC haplotype was associated with a significantly increased risk of GC as compared
with the ATA haplotype (OR = 1.90; 95% CI, 1.11–3.27; P = 0.02).
ConclusionThe results indicate that the gene haplotype of IL-10 may contribute to the susceptibility to GC in the Chinese population.
Key Wordsinterleukin-10-polymorphism-single nucleotide-haplotypes-stomach neoplasms
Clinical Oncology and Cancer Research 7(4):234-239.