The contributing molecular pathways underlying the pathogenesis of
breast cancer need to be better characterized. The principle of our study was to better understand the genetic mechanism of
oncogenesis for human
breast cancer and to discover new possible
tumor markers for use in clinical practice. We used complimentary
DNA (
cDNA) microarrays to compare gene expression profiles of treated Michigan
Cancer Foundation-7 (MCF-7) with recombinant
bromelain and untreated MCF-7. SpringGene analysis was carried out of differential expression followed by Ingenuity Pathway Analysis (IPA), to understand the underlying consequence in developing disease and disorders. We identified 1,102 known genes differentially expressed to a significant degree (p<0.001) changed between the treatment. Within this gene set, 20 genes were significantly changed between treated cells and the control cells with cutoff fold change of more than 1.5. These genes are RNA-binding motif, single-stranded interacting
protein 1 (RBMS1),
ribosomal protein L29 (RPL29),
glutathione S-transferase mu 2 (GSTM2), C15orf32, Akt3, B cell translocation gene 1 (BTG1), C6orf62, C7orf60,
kinesin-associated
protein 3 (KIFAP3), FBXO11, AT-rich interactive domain 4A (ARID4A), COPS2, TBPL1|SLC2A12, TMEM59, SNORD46,
glioma tumor suppressor candidate region gene 2 (GLTSCR2), and LRRFIP. Our observation on gene expression indicated that recombinant
bromelain produces a unique signature affecting different pathways, specific for each congener. The microarray results give a molecular mechanistic insight and functional effects, following recombinant
bromelain treatment. The extent of changes in genes is related to and involved significantly in gap junction signaling,
amyloid processing, cell cycle regulation by BTG family
proteins, and
breast cancer regulation by stathmin1 that play major roles.