Anticancer effects of Curcuma C20-dialdehyde against colon and cervical cancer cell lines

Background: Recent attention on chemotherapeutic intervention against cancer has been focused on discovering and developing phytochemicals as anticancer agents with improved efficacy, low drug resistance and toxicity, low cost and limited adverse side effects. In this study, we investigated the effects of Curcuma C20-dialdehyde on growth, apoptosis and cell cycle arrest in colon and cervical cancer cell lines. Materials and Methods: Antiproliferative, apoptosis induction, and cell cycle arrest activities of Curcuma C20-dialdehyde were determined by WST cell proliferation assay, flow cytometric Alexa fluor 488-annexin V/propidium iodide (PI) staining and PI staining, respectively. Results: Curcuma C20 dialdehyde suppressed the proliferation of HCT116, HT29 and HeLa cells, with IC50 values of 65.4±1.74 μg/ml, 58.4±5.20 μg/ml and 72.0±0.03 μg/ml, respectively, with 72 h exposure. Flow cytometric analysis revealed that percentages of early apoptotic cells increased in a dose-dependent manner upon exposure to Curcuma C20-dialdehyde. Furthermore, exposure to lower concentrations of this compound significantly induced cell cycle arrest at G1 phase for both HCT116 and HT29 cells, while higher concentrations increased sub-G1 populations. However, the concentrations used in this study could not induce cell cycle arrest but rather induced apoptotic cell death in HeLa cells. Conclusions: Our findings suggest that the phytochemical Curcuma C20-dialdehyde may be a potential antineoplastic agent for colon and cervical cancer chemotherapy and/or chemoprevention. Further studies are needed to characterize the drug target or mode of action of the Curcuma C20-dialdehyde as an anticancer agent

Perceptions of Comparative Mind-Body Interventions Among Pregnant Women in Texas

This research aims to analyze perceptions of comparative mind-body interventions among pregnant women in Texas, which can potentially lead to education and/or advocacy on mind-body techniques to improve pregnant women's mental health.Biology and Biochemistry, Department ofHonors Colleg

Comparison of total phenolic content and composition of individual phenolic acids in testae and testa-removed kernels of 15 Valencia-type peanut (Arachis hypogaea L.) genotypes

A successful peanut breeding to obtain genotypes with greater phenolic content requires information on type and content of phenolic compounds in parental peanut genotypes. The aim of this study was to investigate the total phenolic contents and phenolic acid profiles of 15 Valencia-type peanut genotypes both in peanut testae and testa-removed kernels (cotyledons and embryonic axes). Total phenolic content and phenolic acid profiles were analyzed using Folin-Ciocalteu method and high-performance liquid chromatography (HPLC),  respectively. The total phenolic contents of testae and testa-removed kernels varied from 2.47 ± 0.96 to 84.53 ± 5.57 and 0.07 ± 0.01 to 0.12 ± 0.01 mg gallic acid equivalent (GAE)/g dry weight, respectively. Testae of  KK4 and ICG14710 genotypes had the greatest and least total phenolic content, respectively. The peanut  testae with pink color (NM044, NM071, ICG15042 and KK4) had significantly greater phenolic content than those with gray (ICG397 and ICG14710) and yellow (NM001) colors. The present study demonstrates that  p-coumaric and vanillic acids were the two predominant phenolic acids in the testae of nearly all peanut  genotypes tested, except for KK4 genotype whose predominant phenolic acid in its testa was  p-hydroxybenzoic acid. All the testa-removed kernels tested contained significantly greater amount of  p-coumaric acid than other identified phenolic acids. These results would be useful for peanut breeding to  obtain peanut genotypes with greater phenolic acid and other favorable traits.Key words: Valencia peanuts, peanut testae, phenolic acids, p-coumaric acid, vanillic acid

Scopoletin potentiates the anti-cancer effects of cisplatin against cholangiocarcinoma cell lines

Chemotherapy with cisplatin in cholangiocarcinoma produces adverse effects and leads to resistance development by tumors. We aimed to evaluate anti-cancer effects by co-administration of cisplatin and scopoletin in cholangiocarcinoma cells. MTT assay, median effect principle, cell cycle arrest and apoptosis assay were conducted to determine anti-cancer effects. Results revealed that treatment with cisplatin and scopoletin resulted in dose-dependent reduction of cell viability for cholangiocarcinoma cells. Combination of these agents inhibited proliferation of cells significantly more than single agent either. Combination indices reflect additive cytotoxic effect, leading to >2 times dose reduction for each agent. Both the cell cycle arrest (G0/G1) and apoptosis induction underling the enhanced cytotoxicity for the combination. Besides, single agent conferred cell cycle arresting and apoptotic effects in cholangiocarcinoma cells. By contrast, non-cancer cells were less affected with combination. Our observations suggest that cisplatin and scopoletin combination may bring positive significance in cholangiocarcinoma treatment

Transcriptional repression mediated by a novel family of C₂H₂ zinc finger proteins

Two novel and highly related C₂H₂ zinc finger proteins (CTIP1/BCL11A/EVI9 and CTIP2/BCL11B/Rit1) have been implicated in COUP-TF signaling, etiology of myeloid and lymphoid malignancies, and hematopoietic cell development. However, the precise cellular function(s) and the contribution of these proteins to neoplastic processes and hematopoietic cell development remain unknown. The goal of the studies described herein was to elucidate the molecular mechanisms underlying the transcriptional repression mediated by these proteins to understand their biological properties, and ultimately, their cellular function(s). CTIP proteins repressed transcription of a reporter gene in a TSA-insensitive manner, suggesting that this repression mechanism(s) may not involve TSA-sensitive histone deacetylation catalyzed by member(s) of class I and II HDACs. One possible mechanism is that CTIP proteins may exert ISA-insensitive histone deacetylation catalyzed by TSA-insensitive HDAC(s), such as SIRT1, to repress transcription. In deed, SIRT1 was found to interact with CTIP proteins both in vitro and in mammalian cells, and was recruited to the promoter template in a CTIP-dependent manner. The proline-rich regions of CTIP proteins and the sirtuin homology domain of SIRT1 were found to be essential for mediating CTIPs•SIRT1 interactions. Moreover, column chromatography revealed that SIRT1 and CTIP2 were components of a large complex in Jurkat cell nuclear extracts. Based on the findings that SIRT1 associates with CTIP proteins in mammalian cells, SIRT1 may underlie the transcriptional repression activity of CTIP proteins. The following results support the hypothesis that SIRT1 may underlie the mechanism(s) of CTIP-mediated transcriptional repression. First, CTIP-mediated transcriptional repression was inhibited, at least partially, by nicotinamide, an inhibitor of the NAD⁺-dependent, TSA-insensitive HDACs. Second, the decrease in levels of acetylated histones H3 and/or H4 at the promoter region of a reporter gene was observed upon overexpression of CTIP proteins, and this effect was inhibited, at least partially, by nicotinamide. Third, endogenous SIRT1 was recruited to the promoter template of a reporter gene in mammalian cells upon overexpression of CTIP proteins. Fourth, SIRT1 enhanced the transcriptional repression mediated by CTIP proteins and this enhancement required the catalytic activity of SIRT1. Finally, SIRT1 enhanced the deacetylation of template-associated histones H3 and/or H4 in CTIP-transfected cells. In summary, results described herein strongly suggest that CTIP-mediated transcriptional repression involves the recruitment of SIRT1 to the template, at which the TSA-insensitive, but nicotinamide-sensitive histone deacetylase catalyzes deacetylation of promoter-associated histones H3 and/or H4. These results contribute additional understanding to the molecular mechanisms underlying transcriptional activity of CTIP proteins, which might be helpful for identification and characterization of the target genes under the control of CTIP proteins in cells of hematopoietic system and/or the central nervous system

Performance and Emission Characteristics of a Single-Cylinder Diesel Engine Fueled with Yang (Dipterocarpus alatus) Oil

The objective of this study was to determine the performance and emission of diesel engine using Yang (Dipterocarpus alatus) oil compared with conventional diesel fuel. This test was conducted on a single-cylinder diesel engine at 800, 1200, 1600, 2000, and 2400 rpm, then measured and recorded the values. The experimental results showed that torque, brake power and brake thermal efficiency of the engine using Yang oil showed average increased by 5.22%, 5.38% and 4.27%, respectively and brake specific fuel consumption of the engine using Yang oil showed an average decreased by 6.27% compared with those from diesel. The exhaust gas emission of engine using Yang oil were higher than diesel; CO, CO2 and NOx emissions increased slightly by 0.3% Vol., 2.02% Vol. and 18.80 ppm, respectively

Performance and Emission Characteristics of a Single-Cylinder Diesel Engine Fueled with Yang (Dipterocarpus alatus) Oil

846-849The objective of this study was to determine the performance and emission of diesel engine using Yang (Dipterocarpus alatus) oil compared with conventional diesel fuel. This test was conducted on a single-cylinder diesel engine at 800, 1200, 1600, 2000, and 2400 rpm, then measured and recorded the values. The experimental results showed that torque, brake power and brake thermal efficiency of the engine using Yang oil showed average increased by 5.22%, 5.38% and 4.27%, respectively and brake specific fuel consumption of the engine using Yang oil showed an average decreased by 6.27% compared with those from diesel. The exhaust gas emission of engine using Yang oil were higher than diesel; CO, CO2 and NOx emissions increased slightly by 0.3% Vol., 2.02% Vol. and 18.80 ppm, respectively

Increased Expression of Bcl11b Leads to Chemoresistance Accompanied by G1 Accumulation

BACKGROUND: The expression of BCL11B was reported in T-cells, neurons and keratinocytes. Aberrations of BCL11B locus leading to abnormal gene transcription were identified in human hematological disorders and corresponding animal models. Recently, the elevated levels of Bcl11b protein have been described in a subset of squameous cell carcinoma cases. Despite the rapidly accumulating knowledge concerning Bcl11b biology, the contribution of this protein to normal or transformed cell homeostasis remains open. METHODOLOGY/PRINCIPAL FINDINGS: Here, by employing an overexpression strategy we revealed formerly unidentified features of Bcl11b. Two different T-cell lines were forced to express BCL11B at levels similar to those observed in primary T-cell leukemias. This resulted in markedly increased resistance to radiomimetic drugs while no influence on death-receptor apoptotic pathway was observed. Apoptosis resistance triggered by BCL11B overexpression was accompanied by a cell cycle delay caused by accumulation of cells at G1. This cell cycle restriction was associated with upregulation of CDKN1C (p57) and CDKN2C (p18) cyclin dependent kinase inhibitors. Moreover, p27 and p130 proteins accumulated and the SKP2 gene encoding a protein of the ubiquitin-binding complex responsible for their degradation was repressed. Furthermore, the expression of the MYCN oncogene was silenced which resulted in significant depletion of the protein in cells expressing high BCL11B levels. Both cell cycle restriction and resistance to DNA-damage-induced apoptosis coincided and required the histone deacetylase binding N-terminal domain of Bcl11b. The sensitivity to genotoxic stress could be restored by the histone deacetylase inhibitor trichostatine A. CONCLUSIONS: The data presented here suggest a potential role of BCL11B in tumor survival and encourage developing Bcl11b-inhibitory approaches as a potential tool to specifically target chemoresistant tumor cells