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ABSTRACT Objective: In this study, we aimed to evaluate subclinical atherosclerosis in patients with obesity who had cardiovascular disease risk indicators such as arterial stiffness, which is evaluated using pulse wave velocity (PWV), carotid intima-media thickness (CIMT), and biomarkers of endothelial dysfunction such as endocan, ADAMTS97, and ADAMTS9. Subjects and methods: Sixty obese subjects, including 23 subjects with body mass index (BMI) ≥ 40, 37 subjects with BMI ≥ 30 but < 40, and 60 age-and sex-matched control subjects, were included in our study. Serum endocan, ADAMTS97, and ADAMTS9 levels as well as PWV and CIMT measurements of the subjects in the obese and control groups were performed. Results: In the obesity group, PWV levels were significantly higher than they were in the control group and endocan levels were significantly lower than they were in the control group. When we compared the obese group with BMI ≥ 40 and the control group, the BMI ≥ 40 group had significantly higher PWV and CIMT levels than the control group had, whereas endocan, ADAMTS7, and ADAMTS9 levels were similar to those of the control group. When we compared the obese group with BMI ≥ 30 < 40 to the control group, endocan levels were lower in the group with BMI ≥ 30 < 40, and PWV and CIMT levels were similar to the control group. Conclusions: We found that arterial stiffness and CIMT increased in obese patients with BMI ≥ 40 and that increased arterial stiffness was associated with age, systolic blood pressure, and HBA1C. In addition, we found that the endocan levels were lower in obese patients than they were in nonobese control individuals.
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Objective@#To investigate the role of lncRNAs in the invasion and metastasis of salivary adenoid cystic carcinoma (SACC) cells.@*Methods@#With SACC-LM as the experimental group and SACC83 as the control group, lncRNA chips were used to screen the differentially expressed lncRNAs. The differentially expressed lncRNAs were further verified by real-time quantitative RT-PCR (qRT-PCR). The invasion and migration abilities of the adenoid cystic carcinoma cell lines before and after transfection with lncRNA siRNAs were detected by invasion and migration experiments. The clinicopathological features and prognosis of patients with different expression of lncRNAs and SACC were analyzed.@*Results@#The microarray showed that ADAMTS9-AS2 was highly expressed in the SACC-LM cells. Real-time quantitative RT-PCR further confirmed that ADAMTS9-AS2 was significantly upregulated in the SACC-LM cells. Invasion and migration experiments showed that the invasion and migration were significantly reduced after the expression level of ADAMTS9-AS2 was downregulated (P ＜ 0.001). Analysis of the clinicopathological data showed that ADAMTS9-AS2 was highly expressed in SACC. High expression of ADAMTS9-AS2 was associated with poor prognosis and a high tumor metastasis rate in SACC patients.@*Conclusion @#High expression of ADAMTS9-AS2 promotes the migration and invasion of SACC cells. ADAMTS9-AS2 is upregulated in the SACC tissues and is related to a high metastasis rate and poor prognosis.
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Background and purpose: The morbidity of colorectal cancer in China increased year by year. This study aimed to explore the signiifcance of ADAMTS9 protein levels and promoter methylation in colorectal cancer onset and progression. Methods:ADAMTS9 promoter methylation status was detected by methylation speciifc PCR method in 162 colorectal cancer patients’ peripheral blood DNA samples; Plasmatic ADAMTS9 protein levels was detected by enzyme-linked immunosorbent assay method in 162 colorectal cancer patients and 150 healthy subjects. Results: Compared with healthy people, patients with colorectal cancer had a significant lower ADAMTS9 protein level in plasma [(65.25±9.70)μg vs (50.28±9.66)μg, P<0.001];ADAMTS9 gene promoter methylation was observed in 66 among 162 colorectal cancer patients (40.7%);The plasma level of ADAMTS9 protein in patients with methylated ADAMTS9 gene had signiifcantly reduced (P<0.001), while the plasma level of ADAMTS9 protein in patients with low ADAMTS9 protein had signiifcantly increased (P=0.007);ADAMTS9 methylation is closely related to tumor size (larger, P=0.017) and tumor differentiation degree (P=0.029), ADAMTS9 protein low expression is closely related to invasion depth (P=0.020), lymph node metastasis (P=0.019) and Dukes staging (P=0.002).Conclusion: ADAMTS9 protein downregulation induced by DNA promoter methylation may be involved in the pathogenesis, invasion and metastasis, and promote the progression in colorectal cancer.
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Objective: To investigate the aberrant methylation of a disintegrin-like and metalloprotease with thromobospondin type 1 motif 9 (ADAMTS9) gene in human hepatocellular carcinoma tissues, and to explore the correlations of their methylation status with predictive and prognostic significance. Methods: The methylation status of ADAMTS9 gene in 132 cases of hepatocellular carcinoma tissues and their corresponding para-cancerous liver cirrhosis tissues, and 15 cases of normal tissues were detected by methylation specific polymerase chain reaction (MSP). To study the relationship between the gene and the clinical data, the pathological characteristics and survival data of patients were used. Results: Positive rate of ADAMTS9 gene DNA promotor methylation in tumor tissues, para-cancerous liver cirrhosis tissues and the normal tissues were 66.67%, 29.55% and 0.00%, respectively. Significant difference among the three groups was observed (?2 = 49.918,P = 0.000). The positive rate of methylation in tumor tissues was significantly higher than those in para-cancerous liver cirrhosis tissues and the normal tissues. The patients with a portal vein tumor thrombus had a higher methylation-positive rate (78.72%) as compared with the patients without portal vein tumor thrombus (60.00%), and the difference was statistically significant (P = 0.029). The positive rate of ADAMTS9 DNA methylation in the patients with stage ?/? was greater than that in the patients with stage ?/?(P = 0.008). Survival analysis showed that patients with methylation of ADAMTS9 had a lower two-year survival rate (29.5%) than that of the patients with no methylation of ADAMTS9 (50.0%), and the difference was statistically significant (P = 0.002). COX analysis showed that methylation of ADAMTS9 was an independent prognostic factor of hepatocellular carcinoma (P = 0.013). Conclusion: The aberrant methylation of tumor suppressor gene ADAMTS9 DNA promotor may be involved in the formation and progression of hepatocellular carcinoma. These results suggest that the methylation of ADAMTS9 is an independent prognostic factor of hepatocellular carcinoma. Copyright © 2014 by TUMOR.