its antiproliferative effect on Mia-Paca2 cell line

Plant derived products are widely used in cancer treatment. Gall species has been preferred for treatment various diseases in folk medicine, but there are few studies on the anticancer effects of gall species. The present study reports the antioxidant activity and total secondary metabolites of extracts ofA. tomentosusgalls. The antioxidant potency of galls was carried out using differentin-vitromodel systems. Their cytotoxic efficacy on Mia-Paca cell line was also explored. Gall extract was found to contain a large amount of phenolic acids. The extract potently scavenged free radicals including DPPH (IC(50)9.56 +/- 1.08 mu g/mL), ABTS (IC(50)18.51 +/- 0.25 mu g/mL). It can be seen as a potential source of antioxidants according to beta-carotene/linoleic acid method (%92.58 +/- 0.92) and Phosphomolybdenum assays (104.36 +/- 4.95 mgAE/g). Gall extract also posses ability of metal chelating (%40.07 +/- 2.30) and Fe3+(184.01 +/- 2.83 mgTE/g) and Cu2+(89.81 +/- 0.96 mgTE/g) reducing activity. According to total secondary metabolites tests, gall extract showed high total phenolic, total flavonoid and total tannin amount. HPLC analysis of the extract suggested it to contain caffeic acid (424.068.479 mu g/g), ellagic acid (187.696.132 mu g/g). XTT assay revealed gall extract to enhance percent survival of Mia-Paca2 cell line exposedA. tomentosusextracts. The best cytotoxic effect was determined in acetone extracts (IC50: 124.7 mu M). Expression of some genes (Bax, Bcl-2, FAS, BID, caspase-3, caspase-8, caspase-9, caspase-10, FADD, TRADD) in the apoptosis pathway was determined to invastigate apoptosis inducing activity. These results indicate thatA. tomentosusgalls possess potent antioxidant activity, when tested both in chemical as well as biological models.C1 [Kilincarslan Aksoy, Ozge] Pamukkale Univ, Dept Biol, Sci & Art Fac, Denizli, Turkey.[Mammadov, Ramazan] Mugla Sitki Kocman Univ, Dept Mol Biol Genet, Mugla, Turkey.[Secme, Mucahit] TurkeyPamukkale Univ, Med Fac, Dept Med Biol, Denizli, Turkey

A novel oncogene URG4/URGCP and its role in cancer

Oncogenes are mutated form of normal cellular genes called as proto-oncogenes and conduce to the cancer development process. Despite the fact that so many genes have been described, new genes with oncogenic characteristic and potential or tumor supressoring activity are still being defined. Recently, Up-regulated gene 4/Upregulator of cell proliferation (URG4/URGCP), a novel gene, induced by hepatitis-Bvirus-encoded X antigen (HBxAg), has been identified. URG4/URGCP gene was registered to the National Center for Biotechnology Information-GenBank (NCBI-GenBank, Entrez Genelp: 55665 and Entrez Nucleotide ID NM_017920). URG4/URGCP is located on the short arm of chromosome 7 (7p13) and synthesizes a protein containing 922 amino acids in the cytoplas. Relationship between URG4/URGCP expression and clinicopathologic characteristics were evaluated and significant results were in various cancer types such as hepatocellular carcinoma, osteosarcoma, nasopharyngeal carcinoma, bladder cancer, gastric cancer and glioma. Although, biological activity of URG4/URGCP and its effect mechanism in malignant cells is not fully understood, all interesting and promising results shows that URG4/URGCP may be a putative oncogene that contributes to multistep carcinogenesis, cell cycle regulation and other important biological process in the cell

applications on apoptosis and cell cycle in hepatocellular cancer cells

Hepatocellular carcinoma (HCC) is the most common type of liver tumors. There is only one chemodrug for treatment called sorafenib that is an effective multikinase inhibitor. However, most of the patients gain resistance to sorafenib treatment in six months. Thus, there is a limitation for treatment of HCC. Apigenin is a natural flavonoid that has been used for many years as an antioxidant and anti-inflammatory agent. The aim of this study is to investigate the combined therapeutic effects of sorafenib and apigenin upon apoptosis and cell cycle on HepG2 cell line. Cytotoxic effects of sorafenib and apigenin on HepG2 cells were determined by XTT assay. Effects of single and combined treatment on cell migration, invasion and colony formation were analysed by wound healing, transwell matrigel invasion assay and colony formation assay, respectively. TUNEL assay was performed for analyse apoptosis rates. Expression changes of genes related with apoptosis and cell cycle were analysed by quantitative real-time PCR. Combined treatment of sorafenib and apigenin has more decreasing effects on cell viability than single treatment groups. Also, combination group caused significant increase of apoptotic cells. Migration and invasion capability of cells in combined treatment group are decreased. Lastly, quantitative real-time PCR results showed that combination of both drugs arrested cell cycle and increased apoptotic gene expressions more than single treatment groups. This is the first study that investigating the combined treatment of sorafenib and apigenin on HCC in vitro. By combined treatment, apigenin potentiates sorafenib cytotoxicity on HepG2 cells. Effects of combined treatment on migration, invasion, apoptosis and gene expressions showed that may sorafenib and apigenin have synergistic effect.C1 [Sirin, Nazli; Elmas, Levent; Secme, Mucahit; Dodurga, Yavuz] Pamukkale Univ, Fac Med, Dept Med Biol, Denizli, Turkey

efficiencies in patients with schizophrenia and schizoaffective disorder

Schizophrenia and schizoaffective disorder are chronic and debilitating psychiatric disorders. The present study was designed to determine DNA damage in patients with schizophrenia and schizoaffective disorder to assess the roles of oxidative metabolism and DNA repair mechanisms in this process, to assess the contribution of drugs, and thus to demonstrate the differences between schizophrenia and schizoaffective disorder. Thirty schizophrenia and 30 schizoaffective disorder patients, each having at least five years of disease history, aged between 18 and 60 years with no physical or neurological diseases, and 30 healthy volunteers participated in the study. Psychometric scales were applied, and 5 ml of blood was taken from all participants. The DNA damage was measured in lymphocytes by the comet assay method; the total oxidative parameters by ELISA; OGG1 and NEIL1 gene expressions by real-time PCR: and the role of drugs by in vitro assays. The most important finding in this study was that patients with schizophrenia had significantly greater DNA damage than schizoaffective disorder patients and the controls. This study also provides evidence of high oxidative stress statuses and inadequate DNA repair capacities in patients with schizophrenia. Moreover, psychotropic drugs did not induce any DNA damage to the lymphocytes according to in vitro analyses. The use of clozapine and adequate repair processes of the patients were the decisive factors in the prevention of DNA damage. The results of this study provide a reexamination of schizoaffective disorder within the schizophrenia spectrum and indicate that schizoaffective disorder may be considered a different diagnostic category. (C) 2018 Elsevier B.V. All rights reserved

The cytotoxic and genotoxic effects of daidzein on MIA PaCa-2 human pancreatic carcinoma cells and HT-29 human colon cancer cells.

Daidzein (DZ) has anti-inflammatory and antioxidant effects, as well as the dose-dependent inhibition effect on cancer cells. In this study, the cytotoxic and genotoxic effects of DZ on HT-29 (human colorectal adenocarcinoma cells) and MIA PaCa-2 (human pancreatic cancer cells) cell lines were determined using the XTT method and Comet assay, respectively. IC(50) concentrations of DZ were found to be 200 µM in both MIA PaCa-2 and HT-29 cells treated with DZ for 48 hours (h). When the cells were treated with 200 μM of DZ for 48 h, DNA damage was observed in both cell lines. DNA tail length (TL), tail moment (TM), and tail intensity (TI) increased more in MIA PaCa-2 cells treated with 200 μM of DZ than those in the control cell (untreated MIA PaCa-2 cell) group (p < 0.01). However, only DNA-TI and DNA-TM exhibited higher increases in HT-29 cells treated with 200 μM of DZ than those in the control cell (untreated HT-29 cell) group (p < 0.01). This shows that DZ has cytotoxic and genotoxic effects on both cell lines. The observed genotoxic effects of DZ still need to be confirmed in additional future studies

The cytotoxic and genotoxic effects of daidzein on MIA PaCa-2 human pancreatic carcinoma cells and HT-29 human colon cancer cells

Daidzein (DZ) has anti-inflammatory and antioxidant effects, as well as the dose-dependent inhibition effect on cancer cells. In this study, the cytotoxic and genotoxic effects of DZ on HT-29 (human colorectal adenocarcinoma cells) and MIA PaCa-2 (human pancreatic cancer cells) cell lines were determined using the XTT method and Comet assay, respectively. IC50 concentrations of DZ were found to be 200 µM in both MIA PaCa-2 and HT-29 cells treated with DZ for 48 hours (h). When the cells were treated with 200 μM of DZ for 48 h, DNA damage was observed in both cell lines. DNA tail length (TL), tail moment (TM), and tail intensity (TI) increased more in MIA PaCa-2 cells treated with 200 μM of DZ than those in the control cell (untreated MIA PaCa-2 cell) group (p &lt; 0.01). However, only DNA-TI and DNA-TM exhibited higher increases in HT-29 cells treated with 200 μM of DZ than those in the control cell (untreated HT-29 cell) group (p &lt; 0.01). This shows that DZ has cytotoxic and genotoxic effects on both cell lines. The observed genotoxic effects of DZ still need to be confirmed in additional future studies. © 2018 Informa UK Limited, trading as Taylor & Francis Group