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Objective  Immune-related pathways have been frequently associated to tumorigenesis. NOD1 and NOD2 are innate immune receptors responsible for sensing a subset of bacterial-derived components, and to further translate these pathogenic signals through pro-inflammatory and survival pathways. NOD1 and NOD2 have been further associated with tumorigenesis, particularly in gastrointestinal cancers.  NOD1  has also been suggested to be a tumor suppressor gene in a model of estrogen receptor-dependent breast cancer. Contrarily,  NOD2  polymorphisms are associated with higher risk of breast cancer, with no tumor suppressor role being reported. To better delineate this issue, we investigated  NOD1  and  NOD2  expression in a panel of breast cancer cell lines, as well as their potential impact in breast tumorigenesis based on in vitro assays.    Results  The highly invasive Hs578T breast cell line presented the second highest  NOD1  expression and the lowest  NOD2  expression in our panel. Therefore, we investigated whether NOD1 and/or NOD2 might act as a tumor suppressor in this cell model. Our studies indicate that overexpression of either  NOD1  or  NOD2  reduces cell proliferation and increases clonogenic potential in vitro. Elucidation of NOD1 and NOD2 effects on tumor cell viability and proliferation may unveil potential targets for future therapeutic intervention.

Expression and in vitro assessment of tumorigenicity for NOD1 and NOD2 receptors in breast cancer cell lines