• Animal Bioscience
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• v.35 no.4
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• pp.577-586
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• 2022

Objective: The objective of this study was to evaluate the effects of supplementing quercetin extracted from Sophora japonica flower (QS) to the diet of broiler chicks on their growth performance, apparent nutrient digestibility, cecal microbiota, serum lipid profiles, relative organ weight, and breast muscle quality. Methods: A total of 1,088 1-day-old broiler chicks (mixed sex) were randomly assigned to four groups based on the initial body weight (43.00±0.29 g). The experimental period was 35 days (starter, days 0 to 7; grower, days 7 to 21; finisher, days 21 to 35). There were 17 replicate cages per treatment and 16 birds per cage. Dietary treatments consisted of birds receiving basal diet without quercetin as the control group and treatment groups consisted of birds fed basal diet supplemented with 0.2, 0.4, or 0.6 g/kg QS. Results: With the increase of the QS dosage, body weight gain during days 0 to 7 (p = 0.021), 7 to 21 (p = 0.010), and 1 to 35 (p = 0.045), feed intake during days 0 to 7 (p = 0.037) and 1 to 35 (p = 0.025), apparent dry matter digestibility (p = 0.008), apparent energy retention (p = 0.004), cecal lactic acid bacteria counts (p = 0.023), the relative weight of breast muscle (p = 0.014), pH value from breast muscle (p<0.001), and the water holding capacity of breast muscle (p = 0.012) increased linearly, whereas the drip loss from breast muscle (p = 0.001) decreased linearly. Conclusion: The addition of QS in the diet of broiler chicks had positive effects on the breast muscle yield and breast muscle quality, and improved the dry matter digestibility and energy retention by increasing cecal beneficial bacteria counts, thus improving growth performance.

• The Journal of the Korea Contents Association
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• v.14 no.4
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• pp.256-266
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• 2014

Purpose : This study was to explore the long-term effects of breast cancer prevention volunteering on self-efficacy, depression, and posttraumatic growth among survivors with breast cancer. Methods: This pilot study utilized a longitudinal design. Participants were 14 women with breast cancer who participated in the breast cancer prevention educational program The data were collated between February and August in 2013. Self-report questionnaires were used to measure the self-efficacy for self-management of breast cancer, depression, and posttraumatic growth at pre-education(T0), 1 month(T1), 3 months(T2), and 6 months(T1) post-education. A generalized estimating equation regression model was used to identify the effects. Results: The scores of self-efficacy increased significantly at T1(${\chi}^2$=5.56, p=.0l8) and D(${\chi}^2$=4.56, p=.033) compared with T0. Depression and posttraumatic growth remained stable with fairly good levels throughout the 6-month period. Conclusion: The results of this study suggest that breast cancer prevention volunteering in survivors with breast cancer can be effective for enhancing their self-efficacy and maintaining psychological well-bang. Also the study showed that such volunteering activity could be a useful program not only for the general public but also for breast cancer survivors.

• Nutrition Research and Practice
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• v.3 no.2
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• pp.77-83
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• 2009

Retinoic acids (RAs) modulate growth, differentiation, and apoptosis in normal, pre-malignant & malignant cells. In the present study, the effects of RA isomers (all-trans RA, 13-cis RA, and 9-cis RA) on the cell signal transduction of human breast cancer cells have been studied. The relationship between RAs and an enzymatic antioxidant system was also determined. Estrogen-receptor (ER) positive MCF-7 and ER-negative MDA-MB-231 human breast cancer cells were treated with different doses of each RA isomers, all-trans RA, 13-cis RA, or 9-cis RA. Treatment of RA isomers inhibited cell viability and induced apoptosis of MCF-7 cells as a result of increased caspase activity in cytoplasm and cytochrome C released from mitochondria. All-trans RA was the most effective RA isomer in both cell growth inhibition and induction of apoptosis in MCF-7 cells. However, no significant effect of RA isomers was observed on the cell growth or apoptosis in ER-negative MDA-MB-231 cells. In addition, activities of antioxidant enzymes such as catalase and glutathione peroxidase were decreased effectively after treatment of RA in MCF-7 cells, whereas SOD activity was rarely affected. Thus, the present data suggest that all-trans RA is the most potential inducer of apoptosis and modulator of antioxidant enzymes among RA isomers in MCF-7 human breast cancer cells.

• BMB Reports
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• v.52 no.6
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• pp.385-390
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• 2019

Leptin, an adipokine regulating energy metabolism, appears to be associated with breast cancer progression. Insulin-like growth factor-1 (IGF-1) mediates the pathogenesis of breast cancer. The regulation of IGF-1 expression by leptin in breast cancer cells is unclear. Here, we found that leptin upregulates IGF-1 expression at the transcriptional level in breast cancer cells. Activating protein-1 (AP-1)-binding element within the proximal region of IGF-1 was necessary for leptin-induced IGF-1 promoter activation. Forced expression of AP-1 components, c-FOS or c-JUN, enhanced leptin-induced IGF-1 expression, while knockdown of c-FOS or c-JUN abrogated leptin responsiveness. All three MAPKs (ERK1/2, JNK1/2, and p38 MAPK) mediated leptin-induced IGF-1 expression. These results suggest that leptin contributes to breast cancer progression through the transcriptional upregulation of leptin via the MAPK pathway.

• The Journal of the Korea Contents Association
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• v.16 no.11
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• pp.499-509
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• 2016

This study was undertaken to investigate the factors that influence post-traumatic growth in patients with breast cancer. The study subjects were 100 outpatients with breast cancer who visited the outpatient clinic of a university hospital. The instruments used for this study were Korean Post-traumatic Inventory (K-PTGI), Modified Medical Outcomes Study Social Support Survey (mMOS-SS), Self-Efficacy Scale for Self-Management of Breast Cancer (SESSM-B) and Cancer Coping Questionnaire (CCQ). The data were analyzed by t-test, ANOVA, Pearson-correlation coefficient, and stepwise multiple regression using SPSS/WIN 21.0. The mean score of post-traumatic growth was $3.4{\pm}0.9$ out of 5. Post traumatic growth had statistically significant correlation with social support, breast cancer self-management self-efficacy, and coping behavior. In stepwise multiple regression analysis, post-traumatic growth was significantly influenced by therapeutic compliance related self-efficacy and positive reframing coping behavior and it was account for 29% of the total variance. These results suggest that these influencing factors should be considered in developing the nursing intervention to improve the post-traumatic growth in patient with breast cancer.

• KSBB Journal
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• v.32 no.3
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• pp.224-232
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• 2017

Resveratrol has been actively investigated as an anticancer drug since it induces cell growth inhibition and apoptosis in many cancer cells. Resveratrol acts through modulation of multiple pathways and genes. In this study, we found resveratrol reduced cell growth and mammosphere formation in MDA-MB-231 triple-negative human breast cancer cells. This suppressive effect of resveratrol is accompanied by a reduction in Bmi-1 gene expression. We also observed that knock-down of Bmi-1 gene by small interfering RNA effectively sensitizes breast cancer cells to resveratrol treatment. Our data demonstrate, for the first time, that resveratrol down-regulates Bmi-1 expression in human breast cancer cells and suggest that specific molecular targeting of Bmi-1 can be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to resveratrol.

• Natural Product Sciences
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• v.23 no.1
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• pp.35-39
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• 2017

D-chiro-inositol (DCI) is a secondary messenger in insulin signal transduction. It is produced in vivo from myo-inositol via action of epimerase. In this study, we evaluated antitumor activity of DCI against human breast cancer both in vitro and in vivo. In order to determine the inhibitory effects of DCI on growth of human breast cancer cells (MDA-MB-231), two different assessment methods were implemented: MTT assay and mouse xenograft assay. MTT assay demonstrated downturn in cell proliferation by DCI treatment (1, 5, 10, 20 and 40 mM) groups by 18.3% (p < 0.05), 17.2% (p < 0.05), 17.5% (p < 0.05), 18.4% (p < 0.05), and 24.9% (p < 0.01), respectively. Also, inhibition of tumor growth was investigated in mouse xenograft model. DCI was administered orally at the dose of 500 mg/kg and 1000 mg/kg body weight to treat nude mouse for 45 consecutive days. On the 45th day, tumor growth of DCI (500 mg/kg and 1000 mg/kg) groups was suppressed by 22.1% and 67.6% as mean tumor volumes were $9313.8{\pm}474.1mm^3$ and $3879.1{\pm}1044.1mm^3$, respectively. Furthermore, breast cancer stem cell (CSC) phenotype ($CD44^+/C24^-$) was measured using flow cytometry. On the 46th day, CSC ratios of DCI (500 mg/kg) and co-treatment with doxorubicin (4 mg/kg) and DCI (500 mg/kg) group decreased by 24.7% and 53.9% (p < 0.01), respectively. Finally, from tumor recurrence assay, delay of 5 days in the co-treatment group compared to doxorubicin (4 mg/kg) alone group was observed. Based on these findings, we propose that DCI holds potential as an anti-cancer drug for treatment of breast cancer.

• KSBB Journal
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• v.31 no.1
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• pp.52-57
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• 2016

Mutant p53 (R280K) is highly expressed in MDA-MB-231 triple-negative human breast cancer cells. Currently, we reported the role of mutant p53-R280K in mediating the survival of MDA-MB-231 cells in vitro. The present study was undertaken to determine whether mutant p53-R280K affects breast cancer cell growth in vivo. To this end, we used small interfering RNA to knockdown the level of mutant p53-R280K in MDA-MB-231 cells. Silencing of mutant p53-R280K in MDA-MB-231 cells causes substantial tumor regression of established xenografts in vivo. In xenograft model for breast cancer, silencing of mutant p53-R280K in MDA-MB-231 cells significantly inhibited the tumor growth. Moreover, TUNEL assay showed more occurrence of apoptotic cells in mutant p53-R280K silenced tumors compared to control. Our data indicate that mutant p53-R280K has an important role in mediating tumor growth of MDA-MB-231 cells in vivo. Taken together, this study suggests that endogenous mutant p53-R280K could be used as a therapeutic target for breast cancer cells harboring this TP53 missense mutation.

• Korean Journal of Poultry Science
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• v.49 no.1
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• pp.33-43
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• 2022

The present study was conducted to determine the effect of reduced dietary crude protein (CP) with a synthetic indispensable amino acids (AA) supplement on the growth performance, economics, and breast meat quality. A total of 450 male broilers (Ross 308) were used from the age of 7 to 28 days. On d 7, the birds were individually weighed and randomly assigned to three treatment diets with six replicate pens for each treatment in a randomized complete block design. The experimental diets were: (1) a control diet, (2) a diet with a reduction of 1% of the dietary CP with synthetic AA supplements to meet the indispensable AA requirement (OAA) of broiler chickens, and (3) a diet with a reduction of 1% of the dietary CP with synthetic Lys, Met, and Thr supplementation to exceed 5% of the indispensable AA requirement (HAA). There were no differences among the treatments on the final body weight, weight gain, and feed intake. However, the HAA diet impaired the feed conversion ratio at d 21 and during the overall feeding periods (P<0.05). The predicted total feed intake and feed price required to reached 1.5 kg BW was higher than for the birds fed the HAA diet (P<0.05). The breast meat muscle fiber cross sectional area and fiber density varied between the treatments (P<0.05). However, there were no differences in breast meat weight. In conclusion, reducing 1% of dietary CP had no adverse effects on the growth performance or breast meat yields.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.5
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• pp.487-498
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• 2016

Leptin, an adipokine predominantly produced from adipose tissue, is well known to induce tumor growth. However, underlying molecular mechanisms are not established yet. While p53 has long been well recognized as a potent tumor suppressor gene, accumulating evidence has also indicated its potential role in growth and survival of cancer cells depending on experimental environments. In the present study, we examined if p53 signaling is implicated in leptin-induced growth of cancer cells. Herein, we demonstrated that leptin treatment significantly increased p53 protein expression in both hepatic (HepG2) and breast (MCF-7) cancer cells without significant effect on mRNA expression. Enhanced p53 expression by leptin was mediated via modulation of ubiquitination, in particular ubiquitin specific protease 2 (USP2)-dependent manner. Furthermore, gene silencing of p53 by small interfering RNA (siRNA) suppressed leptin-induced growth of hepatic and breast cancer cells, indicating the role of p53 signaling in tumor growth by leptin. In addition, we also showed that knockdown of p53 restored suppression of caspase-3 activity by leptin through modulating Bax expression and prevented leptin-induced cell cycle progression, implying the involvement of p53 signaling in the regulation of both apoptosis and cell cycle progression in cancer cells treated with leptin. Taken together, the results in the present study demonstrated the potential role of p53 signaling in leptin-induced tumor growth.