Regulation of Gap Junction Activators:
Breast cancer patients initially respond to estrogen ablation therapy, but estrogen-independent cells almost always aggressively emerge, and the disease eventually progresses to what is defined as estrogen-independent breast cancer; at which point the tumor is no longer responsive to estrogen ablation therapy, and unrestrained progression of the disease is inevitable. It is believed that restoring gap junction activity is linked to drug sensitivity and reduction of tumorigenicity. Thus, increasing gap junction activity in breast tumor cells provides the targets to enhance anti-neoplastic therapies. Our lab is interested in small molecules that specifically activate gap junction activity and inhibit cancer cell growth.