IL17RB expression might predict prognosis and benefit from gemcitabine in patients with resectable pancreatic cancer.

Background: (Interleukin 17 Receptor Beta) IL17RB has been implicated in several malignancies. However, its role in the progression of and chemosensitivity in pancreatic cancer remains unknown. We aimed to determine the clinical significance of IL17RB expression in the prognosis of resectable pancreatic cancer and in the benefits from gemcitabine treatment.

[Effects of inhibited IGF-IR expression on proliferation and apoptosis of human hepatocellular carcinoma cell lines].

Objective: To investigate the therapeutic value of inhibiting the expression of insulin-like growth factor-I receptor (IGF-IR) using picropodophyllin (PPP) by studying the effects on proliferative and metastatic potentials of human hepatocellular carcinoma (HCC) using an in vitro cultured cell system.

Methods: IGF-IR expression in human HCC cell lines (Bel-7404, Bel-7402, HepG2, and Huh-7) and human hepatocytes (L02) was assessed at baseline (pre-treatment) and after PPP treatment by western blotting. Changes in cell cycle were analyzed by flow cytometry and in cell viability by sulforhodamine B staining.

[Abnormal expression of insulin-like growth factor-II and intervening of its mRNA transcription in the promotion of HepG2 cell apoptosis].

Objective: To explore the expression and pathological features of insulin-like growth factor-II (IGF-II) in tissues and sera of hepatocellular carcinoma (HCC) patients and the siRNA-mediated inhibition of IGF-II mRNA transcription in human HepG2 cells.

Methods: From December 2009 to August 2010, the self-control HCC, paracancerous and distal cancerous tissues were collected to analyze the expression of IGF-II. The serum levels of IGF-II expression were detected for pathological features.

Statins suppress glucose-induced plasminogen activator inhibitor-1 expression by regulating RhoA and nuclear factor-κB activities in cardiac microvascular endothelial cells.

The aim of this study was to investigate the possible proinflammatory signaling pathways involved in statin inhibition of glucose-induced plasminogen activator inhibitor-1 (PAI-1) expression in cardiac microvascular endothelial cells (CMECs). Primary rat CMECs were grown in the presence of 5.7 or 23 mmol/L glucose.

[Correlation between epigenetic alterations in the insulin growth factor-II gene and hepatocellular carcinoma].

To investigate whether epigenetic alterations in the insulin-like growth factor-II (IGF-II) gene that cause differential transcription or expression are correlated with onset and severity of hepatocellular carcinoma (HCC). Patient-matched specimens of HCC, paracancerous, and non-cancerous tissues were collected from 40 primary liver cancer patients. Epigenetic alterations in the promoter (P3) sequence of the IGF-II gene were analyzed by methylation-specific PCR (MSP) and IGF-II transcription was measured by RT-PCR.

[Inhibitory effect of miRNA silencing hypoxia-inducible factor alpha subunit gene on the proliferation of HepG2 cells].

Objective: To investigate the effect of miRNA silencing HIF-1α gene on the proliferation of HepG2 cells.

Methods: The eukaryotic expression plasmids of HIF-1α miRNA and report gene containing hypoxia-reponse element were constructed and transfected into HepG2 cells. The expressions of HIF-1α gene and protein were determined by real time-PCR and Western blotting.

[Dynamic alterations of VEGF and intervention of its expression on effect of hepatocyte malignant transformation].

Objective: To investigate the influences of VEGF expression through the intervention of thalidomide in malignant transformation of hepatocytes.

Methods: Hepatoma model was induced with 2-fluorenyl-acetamide (2-FAA, 0.05%) in male SD rats.

[Expression characteristics of hypoxia inducible factor-1a and its clinical values in hepatocellular carcinoma].

Objective: To investigate the dynamic expression of hypoxia inducible factor-1alpha (HIF-1alpha) and its clinical values in hepatocellular carcinoma (HCC).

Methods: The dynamic changes of liver pathology, HIF-1alpha transcription and expression were observed through the hepatoma model. The self-control specimens from 35 human HCC patients were collected and the expression, cellular distribution, and clinicopathological features of HIF-1alpha and its gene was analyzed by immunohistochemistry, western blotting and nested- PCR, respectively.

Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa B activation pathway in rats.

Background: The active form of nuclear factor-kappa B (NF-kappaB) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignancies. We investigated the dynamic expression of NF-kappaB and its influences on the occurrence of HCC through antiangiogenic (thalidomide) intervention in NF-kappaB activation.

Methods: Hepatoma models were induced with 2-fluorenylacetamide (2-FAA, 0.