ABSTRACT
Curcumin is extracted from turmeric and shows a variety of properties that make it a useful agent for treating diseases and targeting different biological mechanisms, including apoptosis, angiogenesis, inflammation, and oxidative stress. This phenolic compound is safe even at high doses. However, it has poor bioavailability. The incidence rates of endometrial cancer (EC) that is one of the most prevalent gynecological malignancies is increasing. Meanwhile, the onset age of EC has been decreased in past few years. Besides, EC does not show a convenient prognosis, particularly at advanced stages. Based on this information, discovering new approaches or enhancing the available ones is required to provide better care for EC patients. In this review, we cover studies concerned with the anti-tumor effects of curcumin on EC. We focus on molecular mechanisms that are targeted by curcumin treatment in different processes of cancer development and progression, such as apoptosis, inflammation, and migration. Furthermore, we present the role of curcumin in targeting some microRNAs (miRNAs) that may play a role in EC.
ABSTRACT
P-Element induced wimpy testis (PIWI)-interacting RNA (piRNA) is a member of the non-coding RNAs family. Four PIWI proteins are found to be expressed in humans. The number of studies focusing on the roles of piRNAs and PIWI proteins in the field of cancer is increasing. Oral, esophageal, and gastric cancers are considered as important causes of death. PIWI proteins and piRNAs are suggested to be involved in the pathogenesis of these diseases. Thus, studying these molecules may be beneficial for finding new therapeutics. Since it is shown that currently used biomarkers for these cancers have low sensitivity and specificity, there is a necessity for identifying novel non-invasive biomarkers which are highly sensitive and specific. This paper will provide an insight into current knowledge about the functions of PIWI proteins and piRNAs in the oral, esophageal, and gastric cancer. We discuss how PIWI proteins and piRNAs can be involved in the pathogenesis of these cancers. Moreover, we review the studies concerning with the roles of PIWI proteins and piRNAs as biomarkers which are used for diagnostic and prognostic purposes.
Subject(s)
RNA, Small Interfering/genetics , Stomach Neoplasms/diagnosis , Stomach Neoplasms/genetics , Testis/metabolism , Animals , Argonaute Proteins/genetics , Humans , Male , Prognosis , RNA Interference/physiologyABSTRACT
The aim of this systematic review and meta-analysis was to evaluate the effects of resistant starch (RS) on glycemic status, serum lipoproteins and inflammatory markers in patients with metabolic syndrome (MetS) and related disorders. Two independent authors systematically searched online database including EMBASE, Scopus, PubMed, Cochrane Library, and Web of Science from inception until 30 April 2019. Cochrane Collaboration risk of bias tool was applied to assess the methodological quality of included trials. The heterogeneity among the included studies was assessed using Cochrane's Q test and I-square (I2) statistic. Data were pooled using a random-effects model and weighted mean difference (WMD) was considered as the overall effect size. Nineteen trials were included in this meta-analysis. Administration of RS resulted in significant reduction in fasting plasma glucose (FPG) (14 studies) (WMD: -4.28; 95% CI: -7.01, -1.55), insulin (12 studies) (WMD: -1.95; 95% CI: -3.22, -0.68), and HbA1C (8 studies) (WMD: -0.60; 95% CI: -0.95, -0.24). When pooling data from 13 studies, a significant reduction in total cholesterol levels (WMD: -8.19; 95% CI: -15.38, -1.00) and LDL-cholesterol (WMD: -8.57; 95% CI: -13.48, -3.66) were found as well. Finally, RS administration was associated with a significant decrease in tumor necrosis factor alpha (TNF-α) (WMD: -2.02; 95% CI: -3.14, -0.90). This meta-analysis showed beneficial effects of RS on improving FPG, insulin, HbA1c, total cholesterol, LDL-cholesterol and TNF-α levels in patients with MetS and related disorders, but it did not affect HOMA-IR, triglycerides, HDL-cholesterol, CRP and IL-6 levels.
Subject(s)
Inflammation , Metabolic Syndrome , Blood Glucose , Humans , Inflammation/drug therapy , Lipoproteins , Metabolic Syndrome/drug therapy , StarchABSTRACT
Silver nanoparticles (Ag NPs) serve numerous chief functions in cosmetics, engineering, textile, food technology and medicine. These nanoparticles are also utilized in the pharmaceutical industry particularly in the production of novel antimicrobial agents. However, despite the various studies of Ag NPs induced toxicity, there is a lack of information concerning cellular toxicity mechanisms of these nanoparticles on human cells. In the current project, we investigate the anti-cancer effects of Ag NPs in HepG2 (liver hepatocellular adenocarcinoma) cells. The mean particle size and morphology for the prepared nanoparticles were determined by dynamic light scattering (DLS) and transmission electron microscopy (TEM), respectively. Cell viability, reactive oxygen species (ROS) formation, cytochrome c amount and expression level of BAX/CASP 3/CASP 8/CASP 9 were assayed in HepG2 cells after incubation with Ag NPs. The prepared nanoparticles showed the mean particle size of 30.71â¯nm with polydispersity index (PDI) of 0.21. Our results revealed decreased cell viability in a concentration-dependent manner and the IC50 of 75⯵g/mL for Ag NPs. Ag NPs cytotoxicity was associated with induction of ROS and cell apoptosis in HepG2 cell line. According to our findings, Ag NPs could be considered as potential chemotherapeutic agents in the treatment of liver hepatocellular carcinoma.
Subject(s)
Antineoplastic Agents , Apoptosis/drug effects , Carcinoma, Hepatocellular/drug therapy , Liver Neoplasms/drug therapy , Metal Nanoparticles , Silver , Antineoplastic Agents/chemistry , Antineoplastic Agents/pharmacology , Carcinoma, Hepatocellular/metabolism , Carcinoma, Hepatocellular/pathology , Gene Expression Regulation, Neoplastic/drug effects , Hep G2 Cells , Humans , Liver Neoplasms/metabolism , Liver Neoplasms/pathology , Metal Nanoparticles/chemistry , Metal Nanoparticles/therapeutic use , Neoplasm Proteins/biosynthesis , Silver/chemistry , Silver/pharmacologyABSTRACT
INTRODUCTION: Low fetuin-A and 1,25-hydroxyvitamin D3 (vitamin D) levels accompanied with high intact parathyroid hormone (PTH) contents are associated with cardiovascular disease in dialysis patients. The aim of present study was to evaluate the relationship between vitamin D receptor (VDR) gene FokI and ApaI polymorphisms with serum levels of fetuin-A, vitamin D, and intact PTH in hemodialysis patients. MATERIALS AND METHODS: Serum was obtained from 46 stable chronic hemodialysis patients and 43 healthy controls. Serum levels of intact PTH, fetuin-A, vitamin D, calcium, and phosphorus were measured. Genotyping of the VDR gene was performed using standard methods. RESULTS: Serum fetuin-A and vitamin D levels were significantly lower, whereas serum levels of PTH, calcium, and Phosphorus were higher in the hemodialysis patients than in the healthy controls. The FokI genotypes were more frequent in the hemodialysis patients than the control group (P = .004). With respect to FokI genotypes, intact PTH level was higher among the hemodialysis patients compared to the controls (P = .02). In contrast, vitamin D level was lower in the hemodialysis patients with ApaI genotypes compared to the control group (P = .04). CONCLUSIONS: Our study shows that increased serum level of PTH and decreased fetuin-A and vitamin D levels may increase susceptibility of atherosclerosis in patients with hemodialysis through VDR gene FokI and ApaI polymorphisms.