but had no effect on the level of endothelial NO synthase (eNOS) after reperfusion in liver. The 7 d survival rate was significantly higher in C + I/R group than in I/R group. CONCLUSION:Curcumin has protective effects against hepatic I/R injury. Its mechanism might be related to the overexpression of Hsp70 and antioxidant enzymes. Abstract AIM: To investigate the hypothesis that the protective effects of curcumin in hepatic warm ischemia/reperfusion (I/R) injury are associated with increasing heat shock protein 70 (Hsp70) expression and antioxidant enzyme activity. METHODS:Sixty Sprague-Dawley male rats were randomly divided into sham, I/R, C + I/R groups. The model of reduced-size liver warm ischemia and reperfusion was used. Curcumin (50 mg/kg) was administered by injection through a branch of superior mesenteric vein at 30 min before ischemia in C + I/R group. Five rats were used to investigate the survival during 1 wk after operation in each group. Blood samples and liver tissues were obtained in the remaining animals after 3, 12, and 24 h of reperfusion to assess serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), liver tissue NO2 -+ NO3 -, malondialdehyde (MDA) content, superoxide dismutase (SOD), catalase (CAT), nitricoxide synthase (NOS) and myeloperoxidase (MPO) activity, Hsp70 expression and apoptosis ratio. RESULTS:C o m p a r e d w i t h I / R g r o u p , c u r c u m i n pretreatment group showed less ischemia/reperfusioninduced injury. CAT and SOD activity and Hsp70 expression increased significantly. A higher rate of apoptosis was observed in I/R group than in C + I/R group, and a significant increase of MDA, NO2 -+ NO3 -and MPO level in liver tissues and serum transaminase concentration was also observed in I/R group compared to C + I/R group. Curcumin also decreased the activity of inducible NO synthase (iNOS) in liver after reperfusion,

BackgroundPulmonary sarcomatoid carcinoma is a diagnostically challenging group of tumors. It’s a rare histologic subtype of non-small cell lung cancer.There are five subgroups of pulmonary sarcomatoid carcinoma, they are identified as pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma, and pulmonary blastoma. We explored the clinicopathologic features and prognostic factors of this tumor.MethodsWe analyzed retrospectively the clinicopathological data of 51 patients with pulmonary sarcomatoid carcinoma who were treated in the First Affiliated Hospital of Zhengzhou University, Henan Cancer Hospital and Henan People Hospital from January 2005 to December 2012. The correlation between prognosis and age, sex, smoking history, tumor size, TNM staging, and treatment modality was analyzed by the statistical software SPSS 17.0. The survival analysis was conducted using the Kaplan-Meier method. The factors influencing survival were analyzed using univariate (Log-rank) and multivariate (Cox) models.ResultsThe overall survival rates at 1, 2, 3 and 5 years were 45.5%, 35.8%, 28.2% and 20.1%, respectively. Cox univariate analyses revealed that age, tumor size, T stage, M stage, surgery or not, and postoperative chemotherapy or not, were prognostic factors. Cox multivariate analysis found that tumor size and M stage were independent prognostic factors for PSC.ConclusionsDue to its rarity and the lack of large-scale clinical trial evidence, few studies about PSC have been reported, its clinical and pathological characteristics remain unclear, and its preoperative diagnosis and investigation of novel treatment approaches are imperative. In our study, the main factors affecting the prognosis of tumor size and M staging are the crucial prognostic factors for PSC. Surgical resection and postoperative adjuvant chemotherapy might result in better prognosis.

MicroRNAs (miRNAs) have been integrated into cancer development and progression, because they repress translation of target genes which can be tumor suppressors and oncogenes. A number of miRNAs have been found to be closely related to human non-small cell lung cancer (NSCLC). However, the roles of miR-136 in NSCLC are still largely unknown. Here, we show that miR-136 is significantly upregulated in human NSCLC primary tumors and cell lines compared to their nontumor counterparts. Suppression of miR-136 expression in NSCLC cell line A549 inhibited both anchorage-dependent and anchorage-independent proliferation. Further studies showed that suppression of miR-136 expression attenuated phosphorylation of extracellular-signal-regulated kinase 1/2 (Erk1/2). We found that serine/threonine protein phosphatase 2A 55 kDa regulatory subunit B α isoform (PPP2R2A, also known as B55α) was a direct target of miR-136, and suppression of miR-136 expression led to a robust increase in both mRNA and protein levels of PPP2R2A. We found that miR-136 promoted phosphorylation of Erk1/2 through inhibition of PPP2R2A expression, and forced overexpression of PPP2R2A abrogated promotion of Erk1/2 phosphorylation by miR-136. Moreover, forced overexpression of PPP2R2A abrogated the promoting effect of miR-136 on cell growth and led to a reduced growth rate of NSCLC cells. Our findings indicate that miR-136 promotes Erk1/2 phosphorylation through targeting PPP2R2A in NSCLC cells and suggest that it may serve as a therapeutic target in NSCLC therapy.

Accumulating evidence has established that long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) is a tumor regulator in many cancers. Here, we aimed to investigate the possible function of lncRNA PVT1 in esophageal carcinoma (EC) via targeting of microRNA‐145 (miR‐145). Initially, microarray‐based gene expression profiling of EC was employed to identify differentially expressed genes. Moreover, the expression of lncRNA PVT1 was examined and the cell line presenting with the highest level of lncRNA PVT1 expression was selected for subsequent experiments. We then proceeded to examine interaction among lncRNA PVT1, FSCN1, and miR‐145. The effect of lncRNA PVT1 on viability, migration, invasion, apoptosis, and tumorigenesis of transfected cells was examined with gain‐of‐function and loss‐of‐function experiments. We observed that lncRNA PVT1 was robustly induced in EC. lncRNA PVT1 could bind to miR‐145 and regulate its expression, and FSCN1 is a target gene of miR‐145. Overexpression of miR‐145 or silencing of lncRNA PVT1 was revealed to suppress cell viability, migration, and invasion abilities, while also stimulating cell apoptosis. Furthermore, our in vivo results showed that overexpression of miR‐145 or silencing of lncRNA PVT1 resulted in decreased tumor growth in nude mice. In conclusion, our research reveals that down‐regulation of lncRNA PVT1 could potentially promote expression of miR‐145 to repress cell migration and invasion, and promote cell apoptosis through the inhibition of FSCN1. This highlights the potential of lncRNA PVT1 as a therapeutic target for EC treatment.