作者: Gabriel N. Hortobagyi , Mien Chie Hung , Weiya Xia , Lisha Zhang , Yiu Keung Lau
DOI:
关键词: Biology 、 Emodin 、 Tyrosine kinase 、 Receptor tyrosine kinase 、 Tyrosine phosphorylation 、 Endocrinology 、 Cancer cell 、 Tyrosine-kinase inhibitor 、 Internal medicine 、 Cancer research 、 Cell growth 、 Tyrosine
摘要: Overexpression of the HER-2/neu proto-oncogene, which encodes tyrosine kinase receptor p185neu, has been observed in tumors from breast cancer patients. We demonstrated previously that emodin, a inhibitor, suppresses activity HER-2/neu-overexpressing cells and preferentially represses transformation phenotypes these vitro. In present study, we examined whether emodin can inhibit growth mice sensitize to paclitaxel, commonly used chemotherapeutic agent for found significantly inhibited tumor prolonged survival bearing human cells. Furthermore, combination paclitaxel synergistically anchorage-dependent -independent vitro athymic s.c. xenografts expressing high levels p185neu. Both immunohistochemical staining Western blot analysis showed decreases phosphorylation tissue. Taken together, our results suggest is required chemoresistance inhibitors such as also paclitaxel. The may have important implications chemotherapy tumors.