Rabbit Anti-Human PTTG1 (a.a. 121-190) Polyclonal antibody

Background Pituitary tumour-transforming gene (PTTG)-binding factor (PBF), originally known as PTTG1 interacting protein (PTTG1IP), has been found to be significantly increased in well-differentiated thyroid cancer and independently associated with early tumour recurrence. Objective To assess the prognostic significance of PBF expression in a large cohort of papillary thyroid carcinoma (PTC) patients with a long-term follow-up. Design and patients Retrospective analysis of PBF expression in PTC cases at different stages and correlate it with various clinicopathological parameters and patient survival. Subjects included 153 patients who received a thyroid operation for PTC at Chang Gung Memorial Hospital between 1991 and 2000. All patients had a complete follow-up till the end of 2010. Measurements Immunohistochemical study for PBF expression on tissue sections from tumour specimens. Bond automated machine (Leica Microsystems, Germany) with a polyclonal rabbit anti-PBF antibody (LifeSpan BioSciences, LS-C118942, Seattle, WA, USA) was used. SPSS 13.0 for Windows (SPSS Inc, Chicago, IL, USA) was used for all statistical analyses. Results High PBF expression was significantly correlated with age (P = 0.0298), distant metastases at diagnosis (P = 0.0139), tumour multicentricity (P = 0.0035), TNM stage (P = 0.0103), locoregional recurrence (P = 0.0410) and disease-specific mortality (P = 0.0064). The expression level of PBF was significantly correlated with disease-specific survival (P = 0.0065). Cox regression analysis showed that age, tumour size and PBF expression were independent prognostic indicators (P = 0.0097, P = 0.0021 and P = 0.0179). Conclusion PBF expression may be a promising biomarker for prognostic and therapeutic purpose. More large-scale studies are needed to clarify its potential usefulness.

Non-alcoholic steatohepatitis (NASH) is a type of nonalcoholic fatty liver disease and has become a major risk factor for hepatocellular carcinoma (HCC). However, the underlying pathophysiological mechanisms are still elusive. Here, we identify hyaluronan-mediated motility receptor (HMMR) as a critical gene associated with NASH/HCC by combination of bioinformatic analysis and functional experiments. Analysis of differentially expressed genes (DEGs) between normal controls and NASH/HCC identified 5 hub genes (HMMR, UBE2T, TYMS, PTTG1 and GINS2). Based on the common DEGs, analyses of univariate and multivariate Cox regression and the area under the curve (AUC) value of the receiver operating characteristic (ROC) indicate that HMMR is the most significant gene associated with NASH/HCC among five hub genes. Oleate acid (OA), one of fatty acids that induce cellular adipogenesis, stimulates HMMR expression via CCAAT/enhancer-binding protein alpha (CEBP alpha). CEBP alpha increases the expression of HMMR through binding to its promoter. HMMR promotes HCC cell proliferation in vitro via activation of G1/S and G2/M checkpoint transitions, concomitant with a marked increase of the positive cell cycle regulators, including cyclin D1, cyclin E, and cyclin B1. Knockdown of HMMR suppresses HCC tumor growth in nude mice. Our study identifies an important role of HMMR in NASH/HCC, and suggests that HMMR may be a useful target for therapy and prognostic prediction of NASH/HCC patients.