Electronic Thesis/Dissertation
 

In Vivo Investigation of Specific ARID4B Overexpression in Prostate and Mammary Glands

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AT-rich interaction domain 4 B (ARID4B) belongs to the ARID family and is a component of the SIN3A-HDAC corepressor complex. It has been implicated in many cancers, including prostate and breast cancer. However, the mechanism by which ARID4B acts in prostate and breast cancer remains unclear. Prostate cancer and breast cancer is the second leading cancer-causing death of men and women in the United States, respectively. In this study, we investigated how overexpression of ARID4B affects prostate and breast cancer development in vivo. ARID4B was specifically overexpressed in the prostate of male mice and in the mammary gland of female mice. Overexpression of ARID4B in the prostate resulted in high-grade prostatic intraepithelial neoplasia (PIN), which is a precursor for prostate cancer. This suggests that ARID4B may play a role in the progression to prostate cancer. On the other hand, overexpression of ARID4B in the mammary gland did not affect mammary gland development, tumorigenesis, or tumor growth. This may be due to the overexpression of the Erbb2 oncogene and the circulating hormones produced by the ovaries masking the effect of ARID4B. Future studies using ovariectomized mice will be needed to determine whether overexpression of ARID4B can promote mammary gland tumorigenesis under a hormone-deprived condition.

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