Dibromoacetic acid induced Cl.Ly1+2/-9 T-cell apoptosis and activation of MAPKs signaling cascades.

Dibromoacetic acid (DBA), a haloacetic acid by-product of disinfection of drinking water, can cause many adverse effects in test animals, including immunotoxicity. However, the underlying molecular mechanism for the immunomodulatory effects remains unclear. The present study was undertaken to help in defining some potential mechanisms for this type of toxicity.

The effects of icariin on the expression of HIF-1α, HSP-60 and HSP-70 in PC12 cells suffered from oxygen-glucose deprivation-induced injury.

Context: The effects of icariin, a chief constituent of flavonoids from Epimedium brevicornum Maxim (Berberidaceae), on the levels of HIF-1α, HSP-60 and HSP-70 remain unknown.

Objective: To explore the effects of icariin on the levels of HSP-60, HIF-1α and HSP-70 neuron-specific enolase (NSE) and cell viability.

Materials And Methods: PC12 cells were treated with icariin (10, 10 or 10mol/L) for 3 h (1 h before oxygen-glucose deprivation (OGD) plus 2 h OGD).

Dibromoacetic Acid Induces Thymocyte Apoptosis by Blocking Cell Cycle Progression, Increasing Intracellular Calcium, and the Fas/FasL Pathway in Vitro.

Dibromoacetic acid (DBAA), a haloacetic acid found in drinking water as a disinfection by-product, can cause many adverse effects, including immunotoxicity. In a previous study, we confirmed that DBAA can induce obvious immunotoxicity in mice but that the underlying mechanisms are not clearly understood. In our current study, we confirmed that DBAA induced cytotoxicity and apoptosis in thymocytes isolated from mice by a range of DBAA concentrations (0, 5, 10, 20, or 40 μM).

[Transcriptional regulatory properties of DNA sequence upstream of the human ezrin gene promoter in nasopharyngeal carcinoma cells].

Aim: To investigate transcriptional regulatory properties of DNA sequence upstream of the ezrin gene promoter in nasopharyngeal carcinoma CNE2 cells.

Methods: A series of reporter gene expression vectors carrying ezrin-1541/-706 sequence were constructed. In forward or reverse orientation, the ezrin -1541/-706 segment was located upstream of the luc gene in pGL3-Basic, upstream of the ezrin promoter or SV40 promoter, or downstream of the luc gene controlled by ezrin promoter or SV40 promoter.

Identification of the VIL2 enhancer in human embryonic kidney cells.

We previously demonstrated that the VIL2 -87/+134 region exhibited promoter activity in some human cells, and a region further upstream of this promoter might contain an enhancer. However, the properties and location of this VIL2 enhancer remain unclear. In this study, we cloned the VIL2 -1541/-706 segment and investigated its transcriptional regulatory properties via luciferase assays in transiently transfected HEK-293 cells (human embryonic kidney cells).

Specificity protein 1 regulates fascin expression in esophageal squamous cell carcinoma as the result of the epidermal growth factor/extracellular signal-regulated kinase signaling pathway activation.

The overexpression of fascin in human carcinomas is associated with aggressive clinical phenotypes and poor prognosis. However, the molecular mechanism underlying the increased expression of fascin in cancer cells is largely unknown. Here, we identified a Sp1 binding element located at -70 to -60 nts of the FSCN1 promoter and validated that Sp1 specifically bound to this element in esophageal carcinoma cells.

Sp1 and AP-1 regulate expression of the human gene VIL2 in esophageal carcinoma cells.

Ezrin, encoded by VIL2, is a membrane-cytoskeletal linker protein that has been suggested to be involved in tumorigenesis. Ezrin expression in esophageal squamous cell carcinoma (ESCC) was described recently, but its clinical significance and the molecular mechanism underlying its regulated expression remain unclear. Thus, we retrospectively evaluated ezrin expression by immunohistochemistry in a tissue microarray representing 193 ESCCs.

NGALR is overexpressed and regulated by hypomethylation in esophageal squamous cell carcinoma.

Purpose: Neutrophil gelatinase-associated lipocalin receptor (NGALR) mRNA level is reduced in isolated chronic myelogenous leukemia blasts but up-regulated in esophageal squamous cell carcinoma (ESCC). The mechanism of NGALR regulation is unknown. Here, we show the expression pattern of NGALR and examine the aberrant methylation of its gene in ESCC and esophageal carcinoma cell lines.

[Integration and expression of sdh gene in Escherichia coli].

The chloramphenicol-resistant cassette with short shared sequences of ptsG gene on both ends was PCR-generated from plasmid pKF3 and ligated to pMD18-T to construct pMD18-PC. The sdh gene for sorbose dehydrogenase was generated from plasmid pQE60-SDH and inserted into pMD18-PC, then pMD18-PC-SDH was constructed. It was digested with Pvu II and the target fragment ptsG1-cat-sdh-ptsG2 was recovered and electroporated into Escherichia coli JM109/pKD46.