Wistar Factor Model

Therefore, new biomarkers that involve miRNA and cost effective non-invasive treatment options for both BA and HCC must be identified and created. In order to do so, the mechanism behind their development must be further inspected. By studying the interaction between AFB1, miR-155, and Wnt/β-catenin signaling pathway. New research findings will help obtain the information necessary to aid pharmaceutical companies to develop medical products that can help prevent or treat HCC and BA patients. Thus, hundreds of BA birth defects can be prevented and the quality of life in patients will greatly improve.
Hypothesis
We hypothesize that in Wistar rat model, injection of Aflatoxin B1 contributes to a heightened risk of hepatocellular carcinoma by
To explain, rats and or tissue cultures exposed to AFB1 were associated with an upregulation of miR-24 and higher incidence rate of HCC [5] [6]. In addition, certain miRNAs such as miR-27 promoted the activation of Wnt/ β-catenin signaling pathway which adds to cancer growth [7]. If this is the case then other miRNAs such as miR-155 may be induced by AFB1 to play role in creating HCC from BA by way of acting the Wnt/ β-catenin signaling pathway.
Specific Aims and Experimental Procedures
Specific Aim #1: We will determine whether injection of Aflatoxin B1 into a rat will upregulate miR-155 expression in liver tissue.
It is known that miR-155 is overexpressed in HCC tissue but the cause of it remains mysterious. By experimentally testing the effect of AFB1 on miR-155 we will be able to create a link between the two thus providing a cause and effect. If AFB1 increases miR-155 expression, we will know that it may contribute to tumorigenesis of HCC by stimulating proliferation of cancer cells in the liver. Moreover, miR-155 expression can also serve as a potential biomarker to determine if mother and or patient is being exposed to AFB1 and identify individuals who are at high risk of developing the
CCK-8 assay and FITC apoptosis detection kit will detect a low to no cellular proliferation and apoptosis. This is due to AFB1 not being present and therefore not contributing to the upregulation of miR-155. In the case of the experimental rats, RT-qPCR will present a large amount of miR-155 expression levels. Moreover, CCK-8 assay and FITC will show an increased rate of cellular proliferation and a decrease in cellular apoptosis respectively. An indication that AFB1 toxin has a connection with miR-155 in causing HCC. If this was the case, the next step in our research would be to determine if miR-155 causes HCC to develop in BA via the activation of Wnt/β-catenin