Regulation of Breast Cancer Cell Proliferation and Immunity via Targeting Autophagic Process Using siRNA Antagonist Atg-5 in MCF-7 Cells.
Targeting autophagy in breast cancer
Abstract
Background: Breast cancer initiates when normal breast epithelial cells begin to replicate unusually. These cells divide more rapidly than normal cells and continue to be accumulated and formed a lump or mass. Cells may migrate (metastasis stage) from breast tissues to lymph nodes or other human body parts. Cellular autophagy is one of the most critical mechanisms in breast cancer development. Autophagy plays a dual function as a tumor support process or suppressor mechanism. Accordingly, we aimed to highlight the molecular role of autophagy in breast cancer development and cancer therapy using RNA interference (RNAi).
Material and Methods: MCF-7 cell line was used to investigate the direct connection between breast cancer and the autophagy pathway using a respective siRNA antagonist, Atg-5.
Results: MCF-7 cell morphology was markedly influenced by transfection with siRNA antagonist Atg-5 compared with control-transfected and untreated cells. Likewise, the number of liPleving MCF-7 cells reduced in transfected cells with siRNA that antagonist ATG-5, while the relative lactate dehydrogenates (LDH) production significantly increased compared with control-transfected cells. Notably, the knockdown efficiency of Atg-5 gene expression was almost 60% inhibition when the MCF-7 was transfected with the siRNA antagonist Atg-5. Furthermore, the relative gene expression of interleukin -8 (IL-8) and transforming growth factor-beta (TGF-β) downregulated in response to depleted Atg-5 in transfected cells.
Conclusion: Our findings demonstrate that downregulation of Atg-5 leads to sufficient disturbance of autophagic machinery and subsequently regulates breast cancer cell proliferation.
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