Document Detail

Exploration of effects of emodin in selected cancer cell lines: enhanced growth inhibition by ascorbic acid and regulation of LRP1 and AR under hypoxia-like conditions.
MedLine Citation:
PMID:  23212659     Owner:  NLM     Status:  Publisher    
This study explores the link between the antiproliferative activity of emodin through the generation of reactive oxygen species (ROS) in various cancer cell lines and the expression of the androgen receptor (AR) in the prostate cancer cell lines LNCaP (androgen-sensitive) and PC-3 (androgen-refractory), as well as the pro-metastatic low-density lipoprotein receptor-related protein 1 (LRP1) in the above prostate cancer cells and the nonprostate cell lines A549 (lung), HCT-15 (colon) and MG-63 (bone) under normoxic and hypoxia-like conditions. Among all cell lines, emodin showed most growth inhibition in LNCaP, followed by A549. The mechanism of cytotoxicity of emodin was postulated to be the widely reported ROS generation, based on the observations of poor in vitro radical-scavenging activity and increased growth inhibition of emodin by ascorbic acid (AA) pre-treatment owing to the additive effects of ROS generation by emodin and pro-oxidant effects of AA. Emodin downregulated AR in LNCaP under normoxic and hypoxia-like conditions (simulated by CoCl(2) ) and LRP1 under normoxia. Emodin upregulated LRP1 in other cell lines, except HCT-15, under normoxic, and even more markedly under hypoxia-like conditions. The downregulation of AR in LNCaP and upregulation of LRP1 in all cell lines, except HCT-15, under hypoxia-like conditions along with growth inhibition by emodin, suggests that emodin may be a useful therapeutic option against androgen-sensitive prostate cancer and other such LRP1-expressing cancers to attempt the targeting of the elevated LRP1 levels to allow the uptake of emodin and/or any other accompanying therapeutic agents by LRP1. Copyright © 2012 John Wiley & Sons, Ltd.
Shashank Masaldan; Vidhya V Iyer
Related Documents :
21532809 - Ingredients for success: a familial cancer clinic in an oncology practice setting.
24532469 - Clinical significance of the stem cell gene oct-4 in cervical cancer.
23091559 - Dentatin induces apoptosis in prostate cancer cells via bcl-2, bcl-xl, survivin downreg...
23443559 - Lgals3bp regulates centriole biogenesis and centrosome hypertrophy in cancer cells.
24378809 - Fascin1 expression in high-grade serous ovarian carcinoma is a prognostic marker and kn...
24910089 - Phosphofructokinase: a mediator of glycolytic flux in cancer progression.
21532809 - Ingredients for success: a familial cancer clinic in an oncology practice setting.
15003149 - A systematic review of randomized trials in localized prostate cancer.
6193089 - The avoidance of small intestine injury in gynecologic cancer.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-5
Journal Detail:
Title:  Journal of applied toxicology : JAT     Volume:  -     ISSN:  1099-1263     ISO Abbreviation:  J Appl Toxicol     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-5     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8109495     Medline TA:  J Appl Toxicol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012 John Wiley & Sons, Ltd.
Centre for Bio-Separation Technology, VIT University, Vellore, 632014, Tamil Nadu, India.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Initial Combination with Linagliptin and Metformin in Newly Diagnosed Type 2 Diabetes and Severe Hyp...
Next Document:  Comparison of ESWAN, SWI-SPGR, and 2D T2*-Weighted GRE Sequence for Depicting Cerebral Microbleeds.