Open AccessWhole Genome Gene Expression Analysis Reveals Casiopeína-Induced Apoptosis Pathways
Author(s) -
Alejandra Idan Valencia-Cruz,
Laura Uribe-Figueroa,
Rodrigo GalindoMurillo,
Karol Baca-López,
Anllely Grizett Gutiérrez,
Adriana Vázquez-Aguirre,
Lena Ruíz-Azuara,
Enrique HernándezLemus,
Carmen Mejía
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0054664
Subject(s) - hela , apoptosis , dna fragmentation , cancer cell , biology , gene expression profiling , microbiology and biotechnology , gene expression , programmed cell death , computational biology , reactive oxygen species , fragmentation (computing) , genome , cancer research , cell culture , gene , mitochondrion , dna damage , cancer , dna , genetics , ecology
Copper-based chemotherapeutic compounds Casiopeínas, have been presented as able to promote selective programmed cell death in cancer cells, thus being proper candidates for targeted cancer therapy. DNA fragmentation and apoptosis–in a process mediated by reactive oxygen species–for a number of tumor cells, have been argued to be the main mechanisms. However, a detailed functional mechanism (a model) is still to be defined and interrogated for a wide variety of cellular conditions before establishing settings and parameters needed for their wide clinical application. In order to shorten the gap in this respect, we present a model proposal centered in the role played by intrinsic (or mitochondrial) apoptosis triggered by oxidative stress caused by the chemotherapeutic agent. This model has been inferred based on genome wide expression profiling in cervix cancer (HeLa) cells, as well as statistical and computational tests, validated via functional experiments (both in the same HeLa cells and also in a Neuroblastoma model, the CHP-212 cell line) and assessed by means of data mining studies.