Abstract
BackgroundER1626, a novel compound, is a derivate of indeno-isoquinoline ketone. This study was designed to evaluate the biological activity and potential anti-tumor mechanism of ER1626.MethodMTT assay, scratch assay and flow cytometry were used to determine cell proliferation, cell migration and cell cycle distribution as well as cell apoptosis on human breast cancer MCF-7 cells and endometrial cancer Ishikawa cells. We also explored the antiangiogenic effect of ER1626 on HUVEC cells and chicken embryos. The expression of estrogen receptor protein was investigated with western-blot analysis.ResultsER1626 down-regulated the expression of estrogen receptor α protein and up-regulated β protein in MCF-7 and Ishikawa cells. The value of IC50 of ER1626 on MCF-7 and Ishikawa cells were respectively 8.52 and 3.08 µmol/L. Meanwhile, ER1626 decreased VEGF secretion of MCF-7 and Ishikawa cells, disturbed the formation of VEGF-stimulated tubular structure in HUVEC cells, and inhibited the angiogenesis on the chicken chorioallantoic membrane. Scratch assay revealed that ER1626 suppressed the migration of MCF-7, Ishikawa and HUVEC cells. In addition to induction tumor cell apoptosis, ER1626 arrested cell cycle in G1/G0 phase in MCF-7 cells and G2/M phase in Ishikawa cells.ConclusionIn conclusion, our results demonstrated that ER1626 has favorable bioactivities to be a potential candidate against breast cancer and angiogenesis.
Highlights
Breast cancer affects one in eight women during their lives
ER1626 down-regulated the expression of estrogen receptor a protein and up-regulated b protein in MCF-7 and Ishikawa cells
In conclusion, our results demonstrated that ER1626 has favorable bioactivities to be a potential candidate against breast cancer and angiogenesis
Summary
Breast cancer affects one in eight women during their lives. Breast cancer kills more women in the United States than any cancer except lung cancer [1]. Estrogen hormone has been known to play an essential role in the carcinogenesis of breast tumor [3,4] It participates in the physiological and pathological regulation by binding to estrogen receptors (ERs). The mechanism of estrogen action led to the design of antiestrogenic agents which have come to be known as selective estrogen receptor modulators (SERMs). They have been widely used in postmenopausal estrogen therapy in the past decades. SERMs manifest themselves as agonists in some estrogen target tissues while antagonists in others Their selective traits are relative to several factors, including specific tissues, chemical structure, ER subtypes, co-regulators and intracellular signaling pathway, etc [9]. This study was designed to evaluate the biological activity and potential anti-tumor mechanism of ER1626
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