• KOREAN JOURNAL OF CROP SCIENCE
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• v.53 no.1
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• pp.75-84
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• 2008

Colored potatoes are an excellent source of dietary polyphenols including anthocyanins. Generally, anthocyanins from fruits and vegetables exhibit anti-carcinogenesis and anti-cancer properties in vitro test. This experiment was conducted to know the effects of colored potato extracts contained anthocyanins on antimutagenic activity and anticancer activity to six human cancer cell lines containing LNCaP (androgen-dependent) prostate cancer cells. Extracts of three colored potatoes ('Hongyoung', 'Jayoung' and 'Jasim') and the white potato ('Superior') cultivars were used in this study. The extracts of three colored potatoes inhibited the mutagenicities induced by direct mutagen such as 4-nitro-quinoline-1-oxide (4-NQO) and another indirect mutagens of bezo(a)pyrene (BaP). Also, the extracts of 'Hoyoung' and 'Jayoung' showed higher antimutagenic activity than 'Jasim' and 'Superior' against to direct or indirect mutagen on both strains of TA98 and TA100. The activity of growth-inhibitory of extract of four potato cultivars were screened by SRB (sulphorhodamine B) method on diverse human cancer cells representing different types of cancers. Among the extract of four potato cultivars, the extract of 'Jasim' showed moderate inhibition on proliferation of LNCaP, ACHN and MOLT-4F cells and did not inhibit the proliferation of other cancer cells. On the other hand, extract of 'Superior' did not inhibit the proliferation of any tested cancer cell lines. However, the extracts of 'Hongyoung and Jayoung' inhibited the proliferation of cancer cells with $GI_{50}$ values ranging from 2.5 to $30\;{\mu}g/mL$. On the basis of the $GI_{50}$ values, it is clear that LNCaP cells were more sensitive to extracts of colored potato cultivars than other cancer cells. The extract of 'Jayoung' at $30\;{\mu}g/mL$ were more active and inhibited cell proliferation, and induced apoptosis in LNCaP cells. This result revealed that the extracts of colored potatoes are expected to be good candidate for development into source of antimutagenic and anticancer agent.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.323-331
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• 2005

The objective of the present study was to investigate the effect of $\beta-lapachone$, a quinone obtained from the bark of the lapacho tree (Tabebuia avellanedae) in South America, on the cell growth of human hepatoma (HepG2) and bladder (T24) carcinoma cells. Exposure of cancer cells to $\beta-lapachone$ resulted in growth inhibition, morphological changes and apoptosis in a concentration-dependent manner, which could be proved by MTT assay and flow cytometry analysis. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses revealed that $\beta-lapachone$ did not affect the levels of tumor suppressor p53 and cyclin-dependent kinase (Cdk) inhibitor p21 (WAFl/CIPl) expression. However, the transcriptional factor Sp-l and proliferating cell nuclear antigen (PCNA) protein levels were significantly down-regulated by $\beta-lapachone$ in both cell lines. Moreover, $\beta-lapachone$ treatment caused a dose-dependent inhibition of the expression of telomere regulatory gene products such as human telomere reverse transcriptase (hTERT) and telomerase-associated protein-l (TEP-l). Taken together, these findings suggest that $\beta-lapachone$-induced inhibition of human hepatoma and bladder carcinoma cell proliferation is associated with the induction of apoptotic cell death via modulation of several major growth regulatory gene products, and provide important new insights into the additional mechanisms of the anti-cancer activity of $\beta-lapachone$.

• Journal of Life Science
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• v.27 no.9
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• pp.1078-1085
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• 2017

Free radicals have long been considered damaging to various tissues. An excessive amount of reactive oxygen species (ROS) is known to have detrimental effects on the body and to be linked to numerous pathological conditions, such as cardiovascular disease, cancer, diabetes, and skeletal muscle atrophy. On the other hand, recent findings suggest that ROS is important for maintenance and development of cellular activity. Cells respond to increased oxidative stress by adaptive changes in the expression of a variety of proteins involved in the maintenance of cellular integrity. ROS is also essential for skeletal muscle function and metabolism. It is well known that physical exercise has many health benefits. Paradoxically, physical exercise also stimulates the production of ROS, which result in oxidative stress. Based on evidence amassed in the past decade, exercise itself may be considered an antioxidant because training increases the expression of antioxidant enzymes. In this review, we discuss the processes underlying the generation of ROS and its role in exercise-induced adaptation based on recent evidence. Furthermore, we discuss the possible role of NADPH oxidase in exercise-induced activation of insulin signaling and its effect on longevity.

• Journal of Life Science
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• v.15 no.4 s.71
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• pp.528-535
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• 2005

The non-enzymatic anti-oxidants and lunasin peptide from the extracts of the pepper were examined in order to utilize the discovery in natural products as cancer chemopreventive agents. The DPPH (1,1-diphenyl-2-picryl-hydrazyl) free radical scavenging activity on the fruit parts of the pepper was higher than that of the seed, but the difference was low. The Inhibition activity of xanthine/ xanthine oxidase in extracts of the seed was higher than that of the fruit and that of the seed on 20 days after flowering was the highest at the growing period. These were identified as fatty acids and phenolic compounds such as 1-eicosanol, palmitic acid, linoleic acid, linolenic acid and benzonitrile. The contents of fatty acids and phenolic compounds increased according to the time passing at the growing period. Peroxidase (POD) activity of the fruit at middle stage was high than that of other growing stages and that of the seed was the highest at later growing period. Though superoxide dismutase (SOD) activities in fruit were hish by passage of Slowing stage, the activity in seed was low. Lunasin was searched from seeds of the peppers by coomassie blue staining and western blot among them and we just found lunasin peptide from extracted protein of the pepper by western blot. In addition, we observed the contents of lunasin after flowering and confirmed to appear the lunasin at 35 days after flowering. We confirmed that lunasin is complex protein of maturing seeds. 100nM lunasin peptide in pepper showed inhibition effect on colony formation in $2\~12$ cells.

• Journal of Life Science
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• v.31 no.4
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• pp.400-409
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• 2021

Sanguinarine, a natural benzophenanthridine alkaloid, has been considered a potential therapeutic target for the treatment of cancer because it can induce apoptosis in human cancer cells; however, the underlying mechanisms of action still remain unclear. Tumor suppressor p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to anticancer agents. Therefore, in the present study, the role of p53 during apoptosis induced by sanguinarine was investigated in p53wild type (WT, p53+/+) and p53null (p53+/+) HCT116 colon carcinoma cells. Sanguinarine significantly caused greater reductions in cell viability in HCT116 (p53+/+) cells than in HCT116 (p53-/-) cells. Consistently, sanguinarine promoted more DNA damage and apoptosis in HCT116 (p53+/+) cells than in HCT116 (p53-/-) cells while increasing the expression of p53 and cyclin-dependent kinase inhibitor p21^WAF1/CIP1. Sanguinarine increased the activity of caspase-8 and caspase-9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and it activated caspase-3, a typical effect caspase, in HCT116 (p53+/+) cells. Sanguinarine also increased the generation of reactive oxygen species (ROS), and the Bax/Bcl-2 ratio, while destroying the integrity of mitochondria in HCT116 (p53+/+) cells, but not in HCT116 (p53-/-) cells. Overall, the results indicate that sanguinarine induced p53-dependent apoptosis through ROS-mediated activation of extrinsic and intrinsic apoptotic pathways in HCT116 colorectal cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.63 no.3
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• pp.251-260
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• 2007

Purpose: An imbalance of cell proliferation and cell apoptosis is an important mechanism in carcinogenesis. Capase 3, survivin and p53 have been identified as important members of the apoptotic related proteins. This study evaluated the proliferating cell nuclear antigen(PCNA), apoptosis, apoptotic related protein such as capase 3, survivin and p53 using urethane-induced mouse lung carcinogenesis, which provides reproducible steps from hyperplasia to adenocarcinoma. Methods: Urethane was administered to the ICR mice through an intra-peritoneal injection, The mice were sacrificed at 5, 15, and 25 weeks after urethane intervention. The sequential morphological changes and immunohistochemical expression of PCNA, apoptosis, capase 3, survivin, and p53 were examined during mouse lung carcinogenesis. Results: During carcinogenesis, the sequential histological changes were observed from hyperplasia of type II pneumocytes, to anadenoma, and ultimately to an overt adenocarcinoma. The PCNA Labeling index (LI) was 9.6% in hyperplasia, 23.2% in adenoma, and 55.7% in adenocarcinoma, respectively. The apoptotic LI was 0.24% in hyperplasia, 1.25% in adenoma, and 5.27% in adenocarcinoma. A good correlation was observed between the PCNA LI and apoptotic LI. The expression of caspase 3 was remarkable- i.e., 46.7% in adenocarcinoma, in contrast to 15% in hyperplasia and 16% in adenoma. Survivin was detected weakly in the alveolar hyperplasia and showed an increasing expressional pattern in adenoma and adenocarcinoma. p53 expression was detected only in the adenocarcinoma lesions with an expression rate of 13.3%. The level of caspase 3 expression correlated with the increase in the apoptotic index. The positive expression of caspase 3 was associated with an increased apoptotic index. Conclusions: These results suggest that the PCNA LI and apoptotic LI might be useful markers for evaluating the risk of a malignant transformation. In addition, caspase, survivin and p53 might play a role in the early and late steges of urethane-induced mouse lung carcinogenesis.

• The Journal of the Korean bone and joint tumor society
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• v.11 no.1
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• pp.46-53
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• 2005

Purpose: Bisphosphonates (BPs) are the analogues of endogenous pyrophosphates: they have been used in the treatment of skeletal diseases such as Paget's disease, osteoporosis, and tumorinducing ostelysis, and are used in treatment of osteolytic metastasis of breast cancer recently. They are also used as one of the therapeutic agents for metastasis of prostatic cancer of which metastasis makes the mixed nature of osteolysis and ostegenesis. Although the action mechanism of BPs are well known for diseases with excessive osteoclastic bone resorption, the direct effect of BPs has not been known yet. This study was intended to see the tumor suppression capability of Zoledronic acid(ZOL) using nude mouse with osteosarcoma. Materials and Methods: MG-63 and HOS osteosarcoma cell lines were used and the transforemed MG-63-GFP and HOS-GFP cells, which were made for detection under fluorescent light, were subcutaneously injected to make osteosarcoma. The five 6-week male mice were used for the experiment at each group. After the injection, mice were cultivated until tumor pieces grow up to $3{\times}3{\times}3$ $mm^3$ and ZOL of 120 ug/kg was subcutaneously injected twice a week. Sizes of tumor were measured twice a week and photographed under fluorescent light. Results: In in vivo test with HOS osteosarcoma cell lines, mean size of tumors was 2,520 $mm^3$ in control group and was 131 $mm^3$ in ZOL group, which showed 94% of reduction comparing with the control ; with MG-63 osteosarcoma cell lines, mean size of tumors was 2,866 $mm^3$ in control group and was 209 $mm^3$ in test group with 72% of reduction (p<0.05). Conclusion: In in vivo tests with nude mice, we suggest that ZOL has direct effect on osteosarcoma cells and it would be used as one of the therapeutic agents for osteosarcoma, especially to ZOL-sensitive osteosarcoma cells.

• Journal of Life Science
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• v.32 no.7
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• pp.532-541
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• 2022

Obesity induced by high-fat diet (HFD) is verified as a strong risk factor and negative prognostic factor for prostate cancer in several genetically engineered mice although it was not examined in the normal mice. To investigate whether HFD-induced obesity can affect the development and progression of cancer in the prostate of normal mice, alterations in the weight and histological structure of the prostate as well as the expression of cancer-related proteins were analyzed in obese C57BL/6N mice fed with 60% HFD for 16 weeks. First, HFD-induced obesity, including an increase in organ weight, body weight, fat accumulation, and serum lipid profile, was successfully induced in C57BL/6N mice after HFD treatment. The total weight of the prostate significantly increased HFD-induced obesity in the model mice compared with the control group. Among the four lobes of the prostate, the weight of the ventral prostate (VP) and anterior prostate (AP) were higher in HFD-induced obesity model mice than in the control group, although the weights of the lateral prostate (DLP) and seminal vesicle (SV) were constantly maintained. In addition, the incidences of hyperplasia and non-hodgkin's lymphoma (NHL) in the histological structure were remarkably increased in HFD-induced obesity model mice, while the epithelial thickness was higher in the same group. A significant increase in the phosphorylation levels of key proteins in the AKT (protein kinase B) signaling pathway was detected in HFD-induced obesity model mice. Therefore, these results suggest that HFD-induced obesity can promote hyperplasia and NHL in the prostates of C57BL/6N mice through the activation of the AKT signaling pathway.