Predictive value of TRAF6 expression in the efficacy of radiotherapy for esophageal cancer / 国际肿瘤学杂志

Objective:To investigate the predictive value of tumor necrosis factor receptor-associated factor 6 (TRAF6) expression in the efficacy of radiotherapy for patients with esophageal squamous cell carcinoma (ESCC).Methods:A total of 278 patients with ESCC received radical radiotherapy in Yixing Cancer Hospital of Jiangsu Province from February 2012 to March 2015 were included. The expression of TRAF6 in esophageal cancer tissue was detected by immunohistochemistry. The correlations between the expression of TRAF6 and clinicopathological features, short-term efficacy of radiotherapy and survival of ESCC patients were investigated.Results:All the patients were divided into positive expression group ( n=194) and negative expression group ( n=84). TRAF6 expression was significantly associated with TNM stage and lymph node metastasis in ESCC patients ( χ2=13.670, P<0.001; χ2=45.497, P<0.001). The total effective rate of radiotherapy in the TRAF6 positive expression group was 62.9% (122/194), which was significantly lower than that of TRAF6 negative expression group (92.9%, 78/84), and the difference was statistically significant ( χ2=26.085, P<0.001). The median survival time of TRAF positive expression group was 51 months, while that of TRAF negative expression group was not reached, and the difference of survival curve between the two groups was statistically significant ( χ2=7.952, P=0.005). Further analysis showed that higher TNM stage, lymph node metastasis and positive expression of TRAF6 increased the risk of death in ESCC patients ( HR=1.96, 95% CI: 1.39-2.76; HR=1.72, 95% CI: 1.29-2.29; HR=2.31, 95% CI: 1.57-3.39). Conclusion:Patients with TRAF6 positive expression of ESCC have low radiotherapy sensitivity. TRAF6 may be a new target for diagnosis and treatment of ESCC patients, which provides a new idea for the diagnosis, treatment and prognosis of ESCC.

Effect of NF-kappaB on inhibition of non-small cell lung cancer cell cyclooxygenase-2 by brucine / 中国中药杂志

<p><b>OBJECTIVE</b>To study the molecular mechanism of cyclooxygenase-2 (COX-2), one of effective ingredient of brucine, in inducing non-small cell lung cancer cell apoptosis.</p><p><b>METHOD</b>COX-2 promoter, transcription factor deletion mutants and COX-2 mRNA 3'-UTR-containing report plasmids were transfected with Renillia to non-small cell lung cancer A549 cell, in order to detect the activity of report gene luciferase and minimum cis-acting element of COX-2 promoter inhibited by brucine. The influence of brucine on IkappaB phosphorylation and the nuclear translocation of p65 were detected by immunoblotting assay.</p><p><b>RESULT</b>Brucine significantly suppressed LPS-induced COX-2 promoter activation, but revealed minor impact on COX-2 mRNA stability. NF-kappaB in the vicinity of COX-2 promoter-262 was an important cis-acting element of brucine for inhibiting the activity of COX-2 promoter. Brucine was found to inhibit the phosphorylation of IkappaBalpha as well as the nuclear translocation of p65.</p><p><b>CONCLUSION</b>Brucine can improve A549 cells apoptosis by inhibiting the activity of NF-kappaB and the subsequent COX-2 gene expression.</p>

Influence of spleen preservation on hepatic fibrosis and relevant cytokine in rabbits with advanced schistosomiasis / 中国血吸虫病防治杂志

Objective To investigate the effects of spleen preservation on hepatic fibrosis and relevant cytokine in rabbits with advanced schistosomiasis. Methods After hepatic cirrhosis was induced by infecting Schistosoma japonicum cercariae in rabbits, total splenectomy (TSG), subtotal splenectomy (SSG) or sham operation (model control group, MCG) were performed respectively on these rabbits. Meanwhile,a normal control group (NCG) was established. The serum levels of tumor necrosis factor alpha (TNF-α) , interleukin-6 (IL-6) and interleukin-1 beta (IL-lβ) were detected respectively by radioimmunoassay(RIA) at the 8th, 15th and 21st week post-infection. The expressions of transforming growth factor betal (TGF-β1), type Ⅰ and type Ⅲ collagen in liver tissues were determined by immunohistochemistry before and after the operations. Results Compared with NCG, the serum levels of TNF-α, IL-6 and IL-1β of MCG rabbits increased significantly at the 8th week post-infection (P 0.05). The expressions of TGF-β1, type Ⅰ and type Ⅲ collagen in liver tissue of MCG rabbits were significantly higher than those of NCG rabbits before the operation (P 0.05). Conclusion The residual splenic tissue after subtotal splenectomy does not aggravate the hepatic fibrosis at advanced schistosomiasis. The mechanism may be that the relevant cytokines of hepatic fibrosis (TGF-β1, TNF-a, IL-6, IL-1β) decreased to a lower level at this time,and splenectomy does not influence the levels of them.

Study on the effect of brucine on cyclooxygenase 2 in non-small cell lung cancer cells / 中国癌症杂志

Background and purpose:Brucine is one of the active components from Strychnos nux vomica,with signifi cant analgesic,anti-inflammatory and platelet-aggregating inhibitory properties.Due to its cytotoxic effect,the anti-tumor effect of brucine has increasingly been appreciated.In this study,we investigated the impact of brucine on A549 cells proliferation,apoptosis as well as the underlying mechanisms.Methods:MTT assay was used to examine the cell viability,flow cytometric analysis and fluorescent microscope were applied to examine cell apoptosis,ELISA method was used to examine the effect of brucine on PGE2 release from A549 cells and RT-PCR analysis was used to measure mRNA content,western blotting analysis was used to measure protein expression and luciferase activity was detected to examine the effect of brucine on COX-2 promoter activity.Results:Brucine was able to suppress the proliferation of A549 cells and induce cell apoptosis to time-dependent and dose-dependent manner.To understand the mechanisms,COX-2 was identifi ed to be an important target molecule involved in the apoptosis induced by brucine because brucine could suppress the COX-2 mRNA,protein expressions as well as PGE2 release in A549 cells in a timedependent manner.Furthermore,overexpression of COX-2 abrogated brucine-induced cell apoptosis,in contrast,when A549 cells were transfected with COX-2 siRNA,the apoptotic effect of brucine was dramatically enhanced.Further analysis revealed that brucine was able to suppress COX-2 transcriptional activation.Conclusion:Brucine was able to induce lung cancer apoptosis via downregulation of COX-2.