Effect of Trimetazidine on Diabetic Patients with Coronary Heart Diseases: A Meta-Analysis of Randomized, Controlled Trials.

Objective To explore the therapeutic effects of trimetazidine (TMZ) on diabetic patients with coronary heart diseases.Methods We conducted a comprehensive electronic search of PubMed, EMBASE, and Cochrane databases between the inception dates of databases and May 2019 (last search conducted on 30 May 2019) to identify randomized controlled trials. The evaluation method recommended by Cochrane Collaboration for bias risk assessment was employed for quality assessment.

LMP1-augmented kappa intron enhancer activity contributes to upregulation expression of Ig kappa light chain via NF-kappaB and AP-1 pathways in nasopharyngeal carcinoma cells.

Background: Expression of kappa gene is under the control of distinct cis-regulatory elements, including the kappa intron enhancer (iE kappa) and the kappa 3' enhancer (3'E kappa). The active enhancers and expression of immunoglobulin is generally considered to be restricted to B lymphocytes. However, accumulating evidence indicated that epithelial cancer cells, including nasopharyngeal carcinoma (NPC) cell lines, express immunoglobulins.

DNAzymes targeted to EBV-encoded latent membrane protein-1 induce apoptosis and enhance radiosensitivity in nasopharyngeal carcinoma.

Epstein-Barr virus (EBV) is involved in the carcinogenesis of several types of cancers such as nasopharyngeal carcinoma (NPC) and Burkitt's lymphoma. The latent membrane protein (LMP1) encoded by EBV is expressed in the majority of EBV-associated human malignancies and has been suggested to be one of the major oncogenic factors in EBV-mediated carcinogenesis. Therefore, genetic manipulation of LMP1 expression may provide a novel strategy for the treatment of the EBV-associated human cancers.

Phosphorylation and nuclear translocation of STAT3 regulated by the Epstein-Barr virus latent membrane protein 1 in nasopharyngeal carcinoma.

The Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) oncoprotein has been shown to mediate activation of the signal transducer and activator of transcription 3 (STAT3). In the present study, we delineated the mechanism by which LMP1 stimulates STAT3 in a human nasopharyngeal carcinoma (NPC) cell line. LMP1 stimulated STAT3 Tyr 705-dependent nuclear accumulation, as well as the phosphorylation of STAT3 at both Tyr 705 and Ser 727.