[Galectin3 Regulates Transforming Growth Factor-ß-induced Epithelial-mesenchymal].

Objective To explore the role of Galectin3 in transforming growth factor-ß(TGF-ß)-induced epithelial-mesenchymal transition (EMT) in A549 cells. Methods Galectin3 was over-expressed in an A549 cell line. EMT was induced in lung cancer A549 cells by adding TGF-ß. The expressions of Galectin3,E-cadherin,and vimentin were determined by Western blot. The protein expression of E-cadherin and the morphological changes of the cells were detected by immunofluorescence. Cellular proliferation was analyzed with cell counting kit-8,and the cellular migration and invasion was measured by scratches healing and Transwell assay,respectively.Results When only Galectin3 was over-expressed in A549 cell line,the expression levels of EMT-related proteins such as E-cadherin and vimentin were not changed,and the abilities of cellular proliferation,invasion,and migration were not changed either. When the EMT was induced by TGF-ß in A549 cells,the E-cadherin expression was down-regulated and the vimentin expression was up-regulated in A549 cells with Galectin3 over-expression. There was no significant change in cellular proliferation,whereas the abilities of cellular invasion and migration were enhanced.Conclusion The TGF-ß-induced EMT in A549 cells can be enhanced by Galectin3.

Correlation between Plasma Level of Monocyte Chemotactic Protein 1 and Acute Aortic Dissection.

OBJECTIVE: To investigate the potential association between monocyte chemotactic protein 1(MCP-1)in plasma and acute aortic dissection(AAD). METHODS: A total of 110 patients with Stanford type A AAD who had received emergent surgical treatment in Xiangya hospital from September 2011 to September 2014 were enrolled in as the study group;meanwhile,110 patients with simple hypertension who had received treatment in department of cardiology were chosen as the control group. The plasma level of MCP-1 was measured and then compared between these two groups. RESULTS: The plasma level of MCP-1 in the study group was(257.79±86.52)pg/ml,which was significantly higher than that in control group [(136.57±48.84)pg/ml](P<0.001). CONCLUSION: There may be a correlation between plasma MCP-1 level and AAD.

Kank1 reexpression induced by 5-Aza-2'-deoxycytidine suppresses nasopharyngeal carcinoma cell proliferation and promotes apoptosis.

Kank1, which was first described as a potential tumor suppressor for renal cell carcinoma (RCC), mapped to 9p24.3 and encoded an ankyrin-repeat domain-containing protein. Its frequent deletion was found to be associated with several human malignant tumors, cerebral palsy, and neuronal and developmental diseases. However, its functional role in nasopharyngeal cancer (NPC) was still unknown. In the present study, we found that Kank1 expression was down-regulated in NPC cells than in human nasopharyngeal epithelial cell line NP69 and demethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) could improve its mRNA and protein expression level. Further studies demonstrated that DNA methylation might be the mainly cause for Kank1 decreased expression and restored Kank1 expression mediated by 5-aza-CdR played a key role in suppressing NPC cells growth and inducing its apoptosis. Our primary results revealed new function of Kank1 for NPC and implied that epigenetic regulation especially demethylation may have a potential value for NPC treatment.

Association of BTBD7 with Metastasis and Poor Prognosis in Non-Small-Cell Lung Cancer Patients.

Metastasis in lung cancer portends a poor prognosis, and the epithelial-mesenchymal transition (EMT) in lung cancer cells is considered a prerequisite to achieve metastatic potential. Recent studies indicate that BTB/POZ domain-containing protein 7 (BTBD7) regulates EMT-associated proteins in human malignancies and however, the role of BTBD7 in lung cancer have not been identified. In present study, we examined BTBD7 expression status and its association with unfavorable clinical features in non-small-cell lung cancer (NSCLC). Firstly, we studied the fresh specimens, and found that both mRNA and protein expression levels of BTBD7 in NSCLC tissue were significantly increased compared with the adjacent nontumorous lung tissue. Then, we determined BTBD7 protein expressions in the paraffin-embedded samples from NSCLC patients, and analyzed the relations of BTBD7 expression with clinicopathologic features of the patients. The results showed that incidence of metastasis in patients with positive BTBD7 expression was significantly higher than that in those with negative BTBD7 expression, and the positive BTBD7 expression rate in metastatic cases was significantly higher than that in non-metastatic ones; furthermore, Cox regression analyses revealed that BTBD7 was an independent risk factor for either metastasis or survival in NSCLC patients. Thus, we conclude that BTBD7 contributes to metastasis of NSCLC and BTBD7-positive NSCLC may have a high potential for metastasis and thereby a poor prognosis.