Epigenetic modifications such as histone modification play an important role in tumorigenesis. There are several evidence that histone deacetylases (HDACs) play a key role in cancer induction and progression by histone deacetylation. Besides, histone acetylation is being accessed as a therapeutic target because of its role in regulating gene expression. HDAC inhibitors (HDACIs) are a family of synthetic and natural compounds that differ in their target specificities and activities. They affect markedly cancer cells, inducing cell differentiation, cell cycle arrest and cell death, reduction of angiogenesis, and modulation of the immune system. Here, we summarize the mechanisms of HDACs and the HDACIs in several cancers. An online search of different sources such as PubMed, ISI, and Scopus was performed to find available data on mechanisms and pathways of HDACs and HDACIs in different cancers. The result indicated that HDACs induce cancer through multiple mechanisms in various tissues. This effect can be inhibited by HDACIs which affect cancer cell by different pathways such as cell differentiation, cell cycle arrest, and cell death. In conclusion, these findings indicate that the HDACs play a major role in carcinogenesis through various pathways, and HDACIs can inhibit HDAC activity by multiple mechanisms resulting in cell cycle arrest, cell growth inhibition, and apoptosis induction.

Developing a new strategy for an efficient targeted genome editing has always been a great perspective in biology. Although different approaches have been suggested in the last three decades, each one is confronting with limitations. CRISPR-Cas complex is a bacterial-derived system which made a breakthrough in the area of genome editing. This paper presents a brief history of CRISPR genome editing and discusses thoroughly how it works in bacteria and mammalians. At the end, some applications and challenges of this growing research area are also reviewed. In addition to moving the boundaries of genetics, CRISPR-Cas can also provide the ground for fundamental advances in other fields of biological sciences.

Thrombolytic drugs activate plasminogen which creates a cleaved form called plasmin, a proteolytic enzyme that breaks the crosslinks between fibrin molecules. The crosslinks create blood clots, so reteplase dissolves blood clots. Tissue plasminogen activator (tPA) is a well-known thrombolytic drug and is fibrin specific. Reteplase is a modified nonglycosylated recombinant form of tPA used to dissolve intracoronary emboli, lysis of acute pulmonary emboli, and handling of myocardial infarction. This protein contains kringle-2 and serine protease domains. The lack of glycosylation means that a prokaryotic system can be used to express reteplase. Therefore, the production of reteplase is more affordable than that of tPA. Different methods have been proposed to improve the production of reteplase. This article reviews the structure and function of reteplase as well as the methods used to produce it.

Helicobacter pylori is one of the most common human pathogens that can cause gastrointestinal (GI) disorders, including simple gastritis, gastric ulcer, and malignant gastritis. In some cases, such as immunodeficiency and underlying diseases, it can be problematic as opportunistic infections. Diabetes mellitus (type 2) (T2DM) is one of the H. pylori underlying diseases. Since GI problems are observed in diabetic patients, it is necessary to treat H. pylori infection. In this review, we aimed to evaluate the possible relationship between H. pylori and T2DM according to epidemiological surveys of 70 studies retrieved from databases, including Scopus, PubMed, and Google Scholar about the relationship between H. pylori and T2DM, and discuss the reported background mechanisms of this correlation. According to the results of our study, the different studies have shown that H. pylori is more prevalent in Type 2 diabetic patients than healthy individuals or nondiabetic patients. The reason is development of H. pylori infection-induced inflammation and production of inflammatory cytokines as well as different hormonal imbalance by this bacterium, which are associated with diabetes mellitus. On the other hand, by tracing anti-H. pylori antibodies in patients with diabetes mellitus and occurrence of symptoms such as digestive problems in >75% of these patients, it can be concluded that there is a relationship between this bacterium and T2DM. Considering the evidence, it is crucially important that the probability of infection with H. pylori is evaluated in patients with T2DM so that medical process of the patient is followed with higher cautious.