Human WIF1(Wnt inhibitory factor 1) ELISA Kit

The present study aimed to investigate the expression of long non-coding HOX transcript antisense RNA (lncRNA-HOTAIR) in the serum of patients with lymph node metastasis of papillary thyroid carcinoma (PTC) and the underlying mechanism. A total of 89 patients with PTC at Beijing Geriatric Hospital were recruited in this study. Based on the results of color Doppler ultrasound examination, the patients were evaluated for cervical lymph node metastases, and were thereby divided into a metastasis-negative group and a metastasis-positive group. Quantitative fluorescent PCR was used to assess the expression of HOTAIR in serum samples. The PTC cell line TPC-1 was randomly divided into a control and siRNA group. The control group was transfected with a nonsense sequence, while the siRNA group was transfected with si-HOTAIR. After transfection, cell proliferation was evaluated using the MTT assay, and cell migration and invasion were assessed using the cell scratch assay and Transwell assay. Expression levels of vimentin, E-cadherin and proteins associated with the Wnt/beta-catenin signaling pathway were assessed using western blot analysis. Based on the results of the ultrasound examination, 53 patients were allocated to the metastasis-negative group, and 36 to the metastasis-positive group. The expression level of lncRNA-HOTAIR was higher in the metastasis-positive group than that in the metastasis-negative group (P<0.05). Compared with the control group, cell proliferation was reduced while cell migration rate and the number of migrating cells were increased in the siRNA group. Compared with the control group, the expression levels of WIF1 and E-cadherin were significantly increased, while the levels of beta-catenin and vimentin were significantly decreased. In conclusion, lncRNA-HOTAIR is overexpressed in the serum of patients with lymph node metastasis of PTC.In vitroexperiments showed that HOTAIR promoted the proliferation and metastasis of PTC cells by regulating epithelial-mesenchymal transition (EMT) mediated by the Wnt/catenin pathway. Thus, lncRNA-HOTAIR is proposed as a molecular target for the treatment of lymph node metastasis of PTC.

Benzo[a]pyrene (BP) is highly mutagenic and yet does not lead to tumor development in the murine colon. We recently reported the generation of colonic tumors one week after treatment with BP followed by dextran sulfate sodium (DSS), a colitis-inducer. In this BP/DSS model, male CD2F(1) mice were treated orally with BP at 125 mg/kg/day for 5 days, followed by 4% DSS in drinking water for one week. There has been no report so far on the molecular mechanisms involved in tumor development in this model. In the present study, we performed global gene expression analysis on the colonic mucosae obtained from BP-exposed mice one week after treatment with DSS and those treated with the vehicle, BP, or DSS alone. Global gene expression analysis revealed that there were 563 genes preferentially altered (>= 2-fold vs vehicle group) in the colonic mucosae exposed to both BP and DSS. Furthermore, comparative gene expression analysis combined with Ingenuity Pathway Analysis (TM) identified 2 genes associated with Wnt/beta-catenin signaling pathway that were preferentially up-regulated (>= 2-fold vs vehicle group) when BP and DSS were treated in combination in the distal part (site of predilection for tumor induction) of the colonic mucosae, especially in colonic tumors: WNT inhibitory factor 1 (Wif1; 14.6-fold increase) and interferon induced membrane protein 3 (Ifitm3; 5.7-fold increase). In colonic tumors, expression of Wif1 and Ifitm3 proteins were both confirmed by western blot analysis. These findings suggest that these genes are associated with rapid induction of colonic tumors in mice after exposure to BP/DSS, providing insights into the mechanisms of the BP/DSS short-term colon carcinogenesis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.