دورية أكاديمية

Aspirin inhibits growth of ovarian cancer by upregulating caspase-3 and downregulating bcl-2.

التفاصيل البيبلوغرافية
العنوان: Aspirin inhibits growth of ovarian cancer by upregulating caspase-3 and downregulating bcl-2.
المؤلفون: LIN LI, XIAOGANG MAO, XIAOMIN QIN, MIN ZHOU, HUI XING, FAN DONG, XIAOYUAN JIANG, WENHUI ZHUANG
المصدر: Oncology Letters; Jul2016, Vol. 12 Issue 1, p93-96, 4p
مصطلحات موضوعية: ASPIRIN, OVARIAN cancer, OVARIAN tumors, DOWNREGULATION, GENE knockout, CANCER risk factors
مستخلص: The aim of the present study was to investigate the effect and mechanism of different concentrations of aspirin in inhibiting the ovarian cancer of p53N236S gene knockin mice. In total, 28 male p53S mice, with an age range of 4-6 weeks and weight of 20-25 g were selected. The animals were transplanted with SKOV3 cells to establish subdermal human ovarian cancer. The mice were randomly divided into different groups according to the aspirin concentrations (mmol/l) used, i.e., 0, 1, 2 and 3. Subsequently, intraperitoneal injection was performed once every two days for 3 weeks. The tumor volume, lifetime, tumor cell proliferation inhibition rates, caspase-3 protein and bcl-2 protein expression of the four groups were analyzed and compared. Following aspirin treatment for 1, 2 and 3 weeks, the tumor volume of the 3 mmol/l aspirin group was significantly smaller than the other groups (P<0.05). The higher concentration of aspirin led to a smaller tumor size (P<0.05). The cell proliferation inhibition rate of the 3 mmol/l aspirin group was significantly larger than that of other groups (P<0.05). The relative expression level of caspase-3, bcl-2 protein of the 3 mmol/l aspirin group was significantly improved and reduced, respectively. In conclusion, aspirin can inhibit the growth of ovarian cancer of p53S rats due to its upregulation of the expression of caspase-3 protein and downregulation of the expression of bcl-2 protein. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:17921074
DOI:10.3892/ol.2016.4607