Upregulation of microRNA-141 suppresses epithelial-mesenchymal transition and lymph node metastasis in laryngeal cancer through HOXC6-dependent TGF-ß signaling pathway.

Laryngeal cancer is one of the most malignant cancers among the head and neck malignant tumors. Abnormal expression of microRNAs (miRNAs) contributes to cancer development through regulating proliferation and apoptosis of cancer cells. In this study, we aim to explore the roles of microRNA-141 (miR-141), Homeobox C6 (HOXC6) and TGF-ß signaling pathway in epithelial-mesenchymal transition (EMT) and lymph node metastasis in laryngeal cancer. Initially, we identified differentially expressed genes in laryngeal cancer, among which HOXC6 was identified. Then the target miRNA of HOXC6 was predicted and verified. Next, expression of miR-141, HOXC6, TGF-ß1, Smad3, Vimentin and Snail in cancer tissues was detected. Then, AMC-HN-8 cells were transfected with miR-141 mimic, miR-141 inhibitor and HOXC6-siRNA to investigate specific role of miR-141, HOXC6 and TGF-ß signaling pathway in laryngeal cancer in vivo and in vitro. Our results showed that HOXC6 was a target gene of miR-141, which was downregulated in laryngeal cancer. Besides, overexpression of miR-141 could downregulate HOXC6 and inhibit the TGF-ß signaling pathway. Upregulation of miR-141 or silencing of HOXC6 can repress EMT, viability, migration and invasion abilities of laryngeal cancer cells. In addition, upregulation of miR-141 inhibited the tumor growth and lymph node metastasis in vivo. In summary, our findings demonstrated that upregulated miR-141 decreased HOXC6 expression, and inhibited the TGF-ß signaling pathway, EMT and lymph node metastasis in laryngeal cancer, which is of clinical significance in the treatment of laryngeal cancer.

A Primary Investigation on Serum CTX-II Changes in Patients Infected with Brucellosis in Qinghai Plateau, China.

Brucellosis is one of the most widespread zoonotic diseases, with the most frequent complication being osteoarticular changes. The aim of this study was to assess the changes of C-terminal telopeptide of type II collagen (CTX-II) in patients infected with brucellosis. A total of 84 brucellosis patients and 43 volunteers were selected and divided into brucellosis vs. control groups. Serum samples were subjected to serological tests for brucellosis, and CTX-II levels in all samples were measured simultaneously with ELISA. The results showed that serum CTX-II levels in human brucellosis were higher than those of healthy controls, without a statistically significant difference, but serum CTX-II levels in male patients were significantly higher than those of female patients (P<0.05). This finding could indicate the biological changes in the cartilage and bone in human brucellosis.

Functional polymorphisms in the IL-10 gene with susceptibility to esophageal, nasopharyngeal, and oral cancers.

Emerging evidence showed that functional polymorphisms in the IL-10 gene may have effects on individuals' susceptibility to nasopharyngeal, oral and esophageal cancers, yet individually published findings are inconsistent. We therefore designed the meta-analysis to investigate the correlations of IL-10 genetic polymorphisms with susceptibility to nasopharyngeal, oral and esophageal cancers. The EMBASE, MEDLINE, CINAHL, Web of Science and the Chinese Biomedical Database (CBM) databases were searched with no language restrictions. We use Comprehensive Meta-analysis 2.0 software to carry out statistical analysis. Ten case-control studies with a number of 1,883 patients and 2,857 healthy subjects were enrolled. Our results revealed that IL-10 rs1800872 T>G and rs1800896 A>G polymorphisms has a significantly association with the increased risk of esophageal cancer under the allele and dominant models; rs1800871 T>G, rs1800872 T>G and rs1800896 A>G under allele and dominant models could increase the risk of nasopharyngeal cancer; rs1800871T>G, rs1800872T>G and rs1800896 A>G SNPs under allele model were closely related to the susceptibility to oral cancer. Our findings support the point that IL-10 genetic polymorphisms may play essential role in identifying esophageal cancer, nasopharyngeal cancer and oral cancer at early stage.

The Prevention Effect of Selenium on Prevalence of Children Kaschin-Beck Disease in Active Endemic Areas in Qinghai Plateau.

Selenium deficiency is an important environmental risk factor of Kaschin-Beck disease (KBD), and appropriate selenium supplement can reduce the prevalence of KBD. Guide and Xinghai counties, active endemic areas of KBD in Qinghai Plateau, are characteristic with low level of selenium. The aim of this article was to explore the relationship between selenium content and prevalence of children KBD in some active endemic areas from Guide and Xinghai counties. The historical data of KBD were collected, including the detectable rates of KBD and selenium contents of the hair of children, and then the relationship between the prevalence of KBD and selenium contents of hair was analyzed. In KBD endemic areas of Guide County, the detectable rates of X-ray and metaphysic lesion were declined from 25.00 and 16.96% in 2000 to 13.75 and 13.75% in 2010, respectively. Similarly, in KBD endemic areas of Xinghai County, the detectable rates of X-ray and metaphysic lesion were declined from 46.51 and 40.31% in 2000 to 10.64 and 8.51% in 2010, respectively. The selenium contents of hair in Xinghai county were increased from 130.01 ± 48.08 µg/kg in 2003 to 211.8 ± 86.64 µg/kg in 2010(t = 2.98, P < 0.05); the selenium content of hair in Guide County were increased from 142.30 ± 62.02 µg/kg in 2003 to 182.09 ± 78.46 µg/kg in 2010 (t = 3.12, P < 0.05). There was a negative correlation between the prevalence of KBD and selenium contents of hair (r = -0.785). There was a close relationship between selenium content and prevalence of KBD. Selenium could reduce the prevalence of KBD, so it is very necessary to supplement selenium appropriately for KBD prevention.

Selenium: a protective factor for Kaschin-Beck disease in Qing-Tibet Plateau.

There is a close relationship between selenium deficiency and Kaschin-Beck disease (KBD). Although the etiology of KBD is not known and selenium deficiency is not its actual cause, it is an important environmental risk factor. In particular, in the Qing-Tibet Plateau, a selenium-deficient region, the prevalence of KBD is serious and still increasing and continues to damage public health. By providing selenium to the population in appropriate amounts, and especially to children, KBD can be effectively controlled and prevented.