Anti-TIMP2 (native) polyclonal antibody

MicroRNAs (miRNAs), a group of short (similar to 20 nt) non-coding RNAs, play critical roles in the development and progression of ovarian cancer (OC). The role of miR-616, a recently identified cancer-associated miRNA, has never been examined in OC before. The present study demonstrated that the level of miR-616 was increased in OC tissues. A high miR-616 level was associated with poor tumor differentiation and advanced tumor-node-metastasis (TNM) stage. Survival analysis revealed that an elevated level of miR-616 was associated with poor prognosis of OC patients as demonstrated by decreased overall survival (OS) and disease-free survival (DFS). Overexpression of miR-616 promoted the migration, invasion as well as epithelial-mesenchymal transition (EMT) of A2780 cells. Knockdown of miR-616 inhibited these biological functions. Immunohistochemical (IHC) staining revealed that OC tissues with high miR-616 levels exhibited a significantly decreased level of E-cadherin and an increased level of N-cadherin. Furthermore, tissue inhibitor of metalloproteinases 2 (TIMP2) was confirmed to be a direct downstream target of miR-616. Inhibition of TIMP2 expression was required for the promoting effects of miR-616 on the metastasis and EMT of OC cells. Collectively, this study revealed that miR-616 promoted the progression of OC by enhancing cell migration, invasion and EMT.

Long-term exposure to fine particulate matter (PM2.5) may cause adverse pregnancy outcomes but the mechanisms are not clear. Our research confirms that PM2.5 induced DNA damage, and inhibited cell proliferation in HTR-8/SVneo cells, presenting in a dose- and time-dependent manners. Using quantitative proteomics, the 182 and 486 differentially expressed proteins in cells treated with 120 mu g ml(-1) PM2.5 for 24 and 48 h were involved in many critical biological processes, including of cell proliferation, response to DNA damage, regulation of small GTPase mediated signal transduction, and etc. Further validation indicated that PM2.5 blocked the cell cycle at the G2/M phase through activation of the ATR-Cyclin E1/Cdk6 pathway, and it reduced the migration and invasion by upregulating TIMP1 and TIMP2 expression and downregulating Collagen I expression. Our findings were consistent with the observed effects of PM2.5 on cell cycle arrest and inhibition of migration and invasion in human extravillous trophoblast. (C) 2017 Elsevier Inc. All rights reserved.