No abstract

Introduction: Recent experiments have demonstrated that polycomb group gene enhancer zeste homolog 2 (EZH2) is highly expressed in many cancer types. Therefore, we aim to demonstrate EZH2 gene expression in transitional cell bladder cancer. Patients and Methods: The reverse transcriptase-polymerase chain reaction (RT-PCR) was used for detection of EZH2 mRNA levels in healthy and cancerous human bladder specimens. Also, expression of the particular protein was determined by Western blotting and immunohistochemistry to confirm RT-PCR results. Results: Gradually increased expression of EZH2 was detected by mRNA and protein levels in highly advanced bladder cancer specimens. In contrast, 100% of control subjects were negative for EZH2 expression. The expression of EZH2 was more frequent in G3 (92%) than G1-G2 (62–63%) and more frequent in T1-2 (72–85%) than Ta (56%). Western blot analysis results confirm the RT-PCR results. Conclusions: EZH2 overexpression precedes high frequencies of proliferation and the gradual advance of bladder cancer. These observations suggest that deregulated expression of EZH2 is associated with bladder carcinoma.

No abstract

Nitric oxide (NO) is an important molecule that acts in many tissues to regulate a diverse range of physiological processes. It is becoming apparent that NO is a ubiquitous signal in plants. Since the discovery of NO emission by plants in the 1970s, this gaseous compound has emerged as a major signalling molecule involved in multiple physiological functions. Research on NO in plants has gained significant awareness in recent years and there is increasing indication on the role of this molecule as a key-signalling molecule in plants. The investigations about NO in plants have been concentrated on three main fields: The search of NO or any source of NO generation, effects of exogenous NO treatments, NO transduction pathways. However we have limited information about signal transduction procedures by which NO interaction with cells results in altered cellular activities. This article reviews recent advances in NO synthesis and its signalling functions in plants. First, different sources and biosynthesis of NO in plants, then biological processes involving NO signalling are reviewed. NO signalling relation with cGMP, protein kinases and programmed cell death are also discussed. Besides, NO signalling in plant defense response is also examined. Especially NO signalling between animal and plant systems is compared. AbbreviationsABA abscisic acid cGMP cyclic guanosine monophosphate GA gibberellic acid HR hypersensitive response MAPK mitogen activated kinase NO nitric oxide NOS nitric oxide synthase NR nitrite reductase ROS radical oxygen species SAR systemic acquired resistance

Curcumin is assumed to be a plant-derived therapeutic drug that triggers apoptotic cell death in vitro and in vivo by affecting different molecular targets such as NF-κB. Phase I/II trial of curcumin alone or with chemotherapeutic drugs has been accomplished in pancreatic, colon, prostate and breast cancer cases. Recently, autocrine growth hormone (GH) signaling-induced cell growth, metastasis and drug resistance have been demonstrated in breast cancer. In this study, our aim was to investigate the potential therapeutic effect of curcumin by evaluating the molecular machinery of curcumin-triggered apoptotic cell death via focusing on NF-κB signaling and polyamine (PA) metabolism in autocrine GH-expressing MCF-7, MDA-MB-453 and MDA-MB-231 breast cancer cells. For this purpose, a pcDNA3.1 (+) vector with a GH gene insert was transfected by a liposomal agent in all breast cancer cells and then selection was conducted in neomycin (G418) included media. Autocrine GH-induced curcumin resistance was overcome in a dose-dependent manner and curcumin inhibited cell proliferation, invasion-metastasis and phosphorylation of p65 (Ser536), and thereby partly prevented its DNA binding activity in breast cancer cells. Moreover, curcumin induced caspase-mediated apoptotic cell death by activating the PA catabolic enzyme expressions, which led to generation of toxic by-products such as HO in MCF-7, MDA-MB-453 and MDA-MB-231 GH+ breast cancer cells. In addition, transient silencing of SSAT prevented curcumin-induced cell viability loss and apoptotic cell death in each breast cancer cells. In conclusion, curcumin could overcome the GH-mediated resistant phenotype via modulating cell survival, death-related signaling routes and activating PA catabolic pathway.