Abstract
CD44, a cell-adhesion molecule has a dual role in tumor growth and progression; it acts as a tumor suppressor as well as a tumor promoter. In our previous work, we developed a tetracycline-off regulated expression of CD44’s gene in the breast cancer (BC) cell line MCF-7 (B5 clone). Using cDNA oligo gene expression microarray, we identified SOD2 (superoxide dismutase 2) as a potential CD44-downstream transcriptional target involved in BC metastasis. SOD2 gene belongs to the family of iron/manganese superoxide dismutase family and encodes a mitochondrial protein. SOD2 plays a role in cell proliferation and cell invasion via activation of different signaling pathways regulating angiogenic abilities of breast tumor cells. This review will focus on the findings supporting the underlying mechanisms associated with the oncogenic potential of SOD2 in the onset and progression of cancer, especially in BC and the potential clinical relevance of its various inhibitors.
Highlights
Biological Sciences Program, Department of Biological and Environmental Sciences, College of Arts and Department of Basic Medical Science, College of Medicine, QU Health, Qatar University, Biomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha P.O
Tumor cell invasion is the most defining and recurring event during the multistage process of metastasis. It involves the activation of a complex molecular network involving, involving, in particular, cell adhesion molecules (CAMs) [1,2] which facilitate the adhesion of invading cells to their surrounding extracellular matrix (ECM) [3]
This review presents data from the literature supporting our hypothesis that SOD2 might be a novel transcriptional target of CD44-downstream signaling, which promotes
Summary
Tumor cell invasion is the most defining and recurring event during the multistage process of metastasis It involves the activation of a complex molecular network involving, involving, in particular, cell adhesion molecules (CAMs) [1,2] which facilitate the adhesion of invading cells to their surrounding extracellular matrix (ECM) [3]. Four genes have already been validated, and their signaling pathways linking their transcriptional activation to CD44 upstream regulation, have already been published [14]. SOD2 was significantly upregulated upon interaction of CD44 with its major ligand hyaluronan (HA), suggesting that SOD2 might be an additional novel transcriptional target of CD44-downstream signaling that underpins its role in promoting BC tumor cell invasion and metastasis. We have discussed these lines of evidence and proposed a model of the signaling pathways linking CD44 activation by HA to the transactivation of SOD2 to promote breast tumor cell invasion
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