Effect of Pin1 inhibitor juglone on proliferation, migration and angiogenic ability of breast cancer cell line MCF7Adr / 华中科技大学学报(医学)(英德文版)
J. huazhong univ. sci. tech. med. sci
; (6): 531-534, 2015.
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| ID: wpr-250383
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ABSTRACT
This study aimed to evaluate the effects of Pin1 inhibitor Juglone on proliferation, migration and the angiogenic ability of breast cancer cell line MCF7Adr. MCF7Adr cells were cultured and separately treated with Pin1 inhibitor Juglone (treatment group) and DMEM without drug (control group). The cell cycle was examined by flow cytometry. Cell migration was measured by wound-healing assay. Cyclin E protein content was detected by Western blotting. The angiogenesis factor vascular endothelial growth factor (VEGF) in cell media was determined by enzyme linked immunosorbent assay. The results showed that the percentage of cells in G2/M phase in treatment group was significantly higher than that in control group (25.5% vs. 10.1%, P<0.05), and that in G0/G1 phase and S stage in treatment group was significantly lower than that in control group (40.5% vs. 48.2%, and 33.7% vs. 41.7%, P<0.05). Cyclin E protein content in treatment group was significantly lower than that in control group (39.2 ± 7.4 vs. 100 ± 23.1, P<0.05). (A0-A24)/A0 value in treatment group was significantly lower than that in control group (23.9 ± 3.8 vs. 100 ± 14.4, P<0.05). VEGF-A, -B, and -C contents in cell media of treatment group were significantly lower than those in control group (P<0.05). It was suggested that Pin1 inhibitor Juglone can effectively inhibit the proliferation, migration and the angiogenic ability of MCF7Adr cells, and can be used as an alternative drug therapy for breast cancer.
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Asunto principal:
Farmacología
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Neoplasias de la Mama
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Regulación Neoplásica de la Expresión Génica
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Ciclo Celular
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Movimiento Celular
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Naftoquinonas
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Isomerasa de Peptidilprolil
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Ciclina E
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Factor A de Crecimiento Endotelial Vascular
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Proliferación Celular
Límite:
Female
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Humans
Idioma:
En
Revista:
J. huazhong univ. sci. tech. med. sci
Año:
2015
Tipo del documento:
Article