Human HTRA1 (Serine protease HTRA1) ELISA Kit

Background and aims: Epithelial mesenchymal transition (EMT) is involved in the development and progression of cancer. HtrA1 had been showed to play a modulatory role in metastasis of hepatocellular carcinoma (HCC). The relationship between HtrA1 and EMT in HCC was investigated in the present study. Methods: The HtrA1 expression in human HCC tumor tissues and cells was determined by real-time PCR. SiRNA-HtrA1 and pcDNA-HtrA1 were respectively transfected into HepG2 and MHCC97H cells to observe their effects on cell migration and expression of EMT-associated markers Vimentin and E-cadherin. The relationship between HtrA1 and EMT in 60 HCC patients was also investigated. Results: HtrA1 expression of tumor tissues was down-regulated with the increasing of number in lymph nodes metastasis in HCC patients. HtrA1 down-regulation led to the significant increase of cell migration, Vimentin expression and decrease of E-cadherin expression, while HtrA1 overexpression resulted in an opposite function. The HtrA1 expression was positively related to the E-cadherin level (R-2 = 0.5903, P < 0.001) and negatively correlated with Vimentin level (R-2 = 0.6067, P < 0.001) in tumor tissues of HCC, respectively. Conclusion: HtrA1 expression was closely related to EMT, which might be a potential mechanism underlying metastasis of HCC. (C) 2015 Elsevier Inc. All rights reserved.

Schwannomas are common peripheral nerve sheath tumors that can cause debilitating morbidities. We performed an integrative analysis to determine genomic aberrations common to sporadic schwannomas. Exome sequence analysis with validation by targeted DNA sequencing of 125 samples uncovered, in addition to expected NF2 disruption, recurrent mutations in ARID1A, ARID1B and DDR1. RNA sequencing identified a recurrent in-frame SH3PXD2A-HTRA1 fusion in 12/125 (10%) cases, and genomic analysis demonstrated the mechanism as resulting from a balanced 19-Mb chromosomal inversion on chromosome 10q. The fusion was associated with male gender predominance, occurring in one out of every six men with schwannoma. Methylation profiling identified distinct molecular subgroups of schwannomas that were associated with anatomical location. Expression of the SH3PXD2A-HTRA1 fusion resulted in elevated phosphorylated ERK, increased proliferation, increased invasion and in vivo tumorigenesis. Targeting of the MEK-ERK pathway was effective in fusion-positive Schwann cells, suggesting a possible therapeutic approach for this subset of tumors.