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Status |
Public on Jul 01, 2011 |
Title |
Genome-wide transcriptomic profiling of oxaliplatin response |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
Oxaliplatin (OXA) is a member of the family of Pt-containing chemotherapeutic agents that also include cisplatin (CDDP) and carboplatin. OXA is distinguished from these two older drugs by its different spectrum of activity both in preclinical models and in clinical trials. It is the only platinum analogue to have activity in colon cancer, a disease for which this drug has now become a mainstay of therapy. It mainly forms intrastrand adducts between two adjacent guanine residues or guanine and adenine, disrupting DNA replication and transcription. OXA has been reported to be involved in the Nucleotide Excision Repair Pathway (NER), p38 kinase activation, PI3K/AKT pathway and caspase cascade activation through the apoptotic intrinsic pathway. However, not all colon cancer cells show the same sensitivity to OXA. In this study we have compared the changes in RNA expression profiles of colon cancer cell lines with different sensitivity to OXA, determined by IC50.
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Overall design |
The goal of our experiment was to identify genes that are differentially activated or inhibited commparing OXA sensitive and OXA resistent colon cancer cell lines upon OXA treatment. We treated 6 OXA-sensitive colorectal cancer cell lines: LoVo, LS513, SW1116, SW1417, SW48 and LS174TT and 8 resistant cell lines: LS411NN, HCT116, HCT15, SW480, SW948, CACO2, DLD1 and HT29, to identify genes and pathways that could play a role in OXA sensitivity. The experimental design used was “RNA-Reference” and “Dye-Swap”. Each cell line was analyzed in duplicate with RNA reference (Stratagene) as reference sample and labeled each biological condition once by Cy3 and once by Cy5. We took the average of the dye-swapped arrays to cancel the dye effect on any particular gene. In total we used 56 slides.
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Contributor(s) |
Martinez-Cardús A, Martinez-Balibrea E, Malumbres R, Bandres E, Ginés A, Manzano JL, García-Foncillas J, Abad A |
Citation missing |
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Submission date |
Jun 15, 2011 |
Last update date |
Mar 23, 2012 |
Contact name |
Raquel Malumbres |
E-mail(s) |
rmalumbres@yahoo.com
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Phone |
+34 948194700
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Organization name |
University of Navarra/ Clínica Universidad de Navarra
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Department |
Hemato-Oncology
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Lab |
Multiple Myeloma
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Street address |
Avenida Pio XII 55
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City |
Pamplona |
State/province |
Navarra |
ZIP/Postal code |
31008 |
Country |
Spain |
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Platforms (1) |
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Samples (28)
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GSM742778 |
Control LS174T colon cancer cells |
GSM742779 |
Control LS411N colon cancer cells |
GSM742780 |
Control LS513 colon cancer cells |
GSM742781 |
Control SW48 colon cancer cells |
GSM742782 |
Control SW1417 colon cancer cells |
GSM742783 |
Control HCT15 colon cancer cells |
GSM742784 |
Control SW1116 colon cancer cells |
GSM742785 |
Control CACO2 colon cancer cells |
GSM742786 |
Control SW948 colon cancer cells |
GSM742787 |
Control SW480 colon cancer cells |
GSM742788 |
Control HCT116 colon cancer cells |
GSM742789 |
OXA treated DLD11 colon cancer cells |
GSM742790 |
OXA treated HT29 colon cancer cells |
GSM742791 |
OXA treated LoVo colon cancer cells |
GSM742792 |
OXA treated LS174T colon cancer cells |
GSM742793 |
OXA treated LS411N colon cancer cells |
GSM742794 |
OXA treated LS13 colon cancer cells |
GSM742795 |
OXA treated SW48 colon cancer cells |
GSM742796 |
OXA treated SW1417 colon cancer cells |
GSM742797 |
OXA treated HCT15 colon cancer cells |
GSM742798 |
OXA treated SW1116 colon cancer cells |
GSM742799 |
OXA treated CACO2 colon cancer cells |
GSM742800 |
OXA treated SW948 colon cancer cells |
GSM742801 |
OXA treated SW480 colon cancer cells |
GSM742802 |
OXA treated HCT116 colon cancer cells |
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Relations |
BioProject |
PRJNA143685 |
Supplementary file |
Size |
Download |
File type/resource |
GSE30011_RAW.tar |
108.6 Mb |
(http)(custom) |
TAR (of TXT) |
Processed data included within Sample table |
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