Oxaliplatin induces different cellular and molecular chemoresistance patterns in colorectal cancer cell lines of identical origins

Cancer cells frequently adopt cellular and molecular alterations and acquire resistance to cytostatic drugs. Chemotherapy with oxaliplatin is among the leading treatments for colorectal cancer with a response rate of 50%, inducing intrastrand cross-links on the DNA. Despite of this drug's effic...

Full description

Saved in:
Bibliographic Details
Published in:BMC genomics 2013-07, Vol.14 (1), p.480-480
Main Authors: Virag, Piroska, Fischer-Fodor, Eva, Perde-Schrepler, Maria, Brie, Ioana, Tatomir, Corina, Balacescu, Loredana, Berindan-Neagoe, Ioana, Victor, Bogdan, Balacescu, Ovidiu
Format: Article
Language:English
Subjects:
Antineoplastic Agents - pharmacology
Cancer therapies
Cell Line, Tumor
Cell Movement - drug effects
Cell Movement - genetics
Colorectal cancer
Colorectal Neoplasms - pathology
Cross-Linking Reagents - pharmacology
Cytotoxicity
DNA repair
Drug Resistance, Neoplasm - genetics
Drug therapy
Gene expression
Genetic aspects
Genomics
Health aspects
Humans
Instrument industry
Ionizing radiation
Metastasis
Neoplasm Invasiveness
Organoplatinum Compounds - pharmacology
Phenotype
Reproducibility of Results
Software
Stem cells
Time Factors
Transcriptome - drug effects
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cancer cells frequently adopt cellular and molecular alterations and acquire resistance to cytostatic drugs. Chemotherapy with oxaliplatin is among the leading treatments for colorectal cancer with a response rate of 50%, inducing intrastrand cross-links on the DNA. Despite of this drug's efficiency, resistance develops in nearly all metastatic patients. Chemoresistance being of crucial importance for the drug's clinical efficiency this study aimed to contribute to the identification and description of some cellular and molecular alterations induced by prolonged oxaliplatin therapy. Resistance to oxaliplatin was induced in Colo320 (Colo320R) and HT-29 (HT-29R) colorectal adenocarcinoma cell lines by exposing the cells to increasing concentrations of the drug. Alterations in morphology, cytotoxicity, DNA cross-links formation and gene expression profiles were assessed in the parental and resistant variants with microscopy, MTT, alkaline comet and pangenomic microarray assays, respectively. Morphology analysis revealed epithelial-to-mesenchymal transition in the resistant vs parental cells suggesting alterations of the cells' adhesion complexes, through which they acquire increased invasiveness and adherence. Cytotoxicity measurements demonstrated resistance to oxaliplatin in both cell lines; Colo320 being more sensitive than HT-29 to this drug (P 
ISSN:1471-2164
1471-2164
DOI:10.1186/1471-2164-14-480