Abstract
Introduction: Resistance to chemotherapy continues to impede treatment of hormone receptor negative breast cancer patients. Investigation into the etiology of this resistance shows that GPR30 may participate in communicating downstream signals of growth and proliferation that are traditionally signaled through the estrogen and progestin receptors. Knockdown of GPR30 may aid in diminishing these alternative signaling cascades and therefore allow standard chemotherapeutics to not only hinder proliferation but succeed in promoting cell death.
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