Interferon-γ regulates cell malignant growth via the c-Abl/HDAC2 signaling pathway in mammary epithelial cells

摘要: Interferon-γ (IFN-γ) has been used to control cancers in clinical treatment. However, an increasing number of reports have suggested that some cases effectiveness declines after a long treatment period, the reason being unclear. We reported previously long-term IFN-γ induces malignant transformation healthy lactating bovine mammary epithelial cells (BMECs) vitro. In this study, we investigated mechanisms underlying proliferation BMECs under The primary study were stimulated by (10 ng/mL) for term promote malignancy. observed could cell proliferation, increase expression cyclin D1/cyclin-dependent kinase 4 (CDK4), decrease p21, and upregulate cellular-abelsongene (c-Abl) histone deacetylase 2 (HDAC2). HDAC2 inhibitor, valproate (VPA) c-Abl imatinib, lowered level D1/CDK4, increased leading inhibitory effect on IFN-γ-induced growth. When was downregulated, also decreased promoted proteasome degradation. These data suggest promotes growth through c-Abl/HDAC2 signaling pathway. Our findings application may be closely associated with promotion even carcinogenesis breast cancer.