Investigating the Function of ARID4B in Anti-tumor Immunity in Breast Cancer
Open Access DepositedBreast cancer is the second-leading cause of cancer death and most common cancer in women in the United States. In this study, AT-rich interaction domain 4B (ARID4B) was investigated as it has been implicated in many cancers, including breast cancer. Its mechanism, however, remains unclear. The effects of ARID4B on cell proliferation and tumor growth were investigated using MTT assays and a syngeneic mouse model, respectively. This study was conducted by utilizing control murine breast carcinoma cell lines and their Arid4b knockout (Arid4bKO) pair. The results of the MTT assays indicated that ARID4B plays a role in cell proliferation as the Arid4bKO cells exhibited a lower proliferation rate compared to the control cells. This relation was partially reflected in the mouse models considering those that received the control cells exhibited progressive tumor growth throughout the entire experimental period. However, those that received the Arid4bKO cells exhibited significantly lower tumor growth rates and tumor volumes, and the tumors began to shrink midway through the experiment. The difference observed between the in vitro and in vivo study lead to the hypothesis that ARID4B regulates tumor growth in part by impinging on tumor immunity. To test this hypothesis, immunohistochemistry (IHC) was used to investigate what immune cells are involved in vivo. IHC results revealed that there was increased apoptosis as well as infiltration of Helper and Cytotoxic T cells, M1 macrophages, and Interferon-gamma cytokines in the Arid4bKO tumors compared to the control tumors. Whereas the control tumors exhibited greater cell proliferation and M2 macrophages compared to the Arid4bKO tumors. These results together support the hypothesis that ARID4B is involved in anti-tumor immunity.
- All rights reserved
Notice to Authors
If you are the author of this work and you have any questions about the information on this page, please use the Contact form to get in touch with us.