• Korean Journal of Microbiology
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• v.44 no.4
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• pp.277-281
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• 2008

HIV affects many organ systems. Patients with HIV infection have substantially increased risk of developing various cancers, primarily by opportunistic infection with oncogenic viruses due to their immunocompromised status. However, extensive evidence also indicates that the viral protein, Tat itself, may playas a major factor in the development of AIDS-related neoplasms. The molecular mechanism underlying Tat's oncogenic activity may include deregulation of cellular genes. Therefore, in this study, we examined the effect of HIV-l Tat on CD99 as one of the target cellular genes, which is a well-known tumor marker in several cancers. By using established HeLa clones that are stably expressing Tat, we found that CD99 is upregulated by endogenous Tat, whereas STAT3 is down regulated. Upon the screening of genes differentially expressed between Tat-stable cells and the control cells by using the gene fishing technique, DEG, we detected 3 genes which expression is affected by the presence of Tat. Furthermore, the methylation specific PCR analysis of the stably Tat expressing cell lines revealed that the CD99 promoter is de methylated in the presence of Tat. Taken together, these results open a potential role of CD99 in AIDS-related oncogenesis via epigenetic regulation by HIV-1 Tat.

• Journal of Food Hygiene and Safety
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• v.34 no.3
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• pp.303-308
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• 2019

L-carnitine is found in high levels in muscle tissues. It has been developed as a nutrient and dietary supplement, and also used as a therapeutic supplement in various diseases including type II diabetes, osteoporosis and metabolic neuropathies. However, it is not fully understood how it affects cellular mechanisms in colorectal cancer. Therefore, we attempted to determine the effect of L-carnitine in HCT116 human colorectal cancer cells. First, the HCT116 cells were exposed to L-carnitine for 24 hours at 0-40 mM, and then analyzed for cellular proliferation, oxidative stress and related mechanisms. In a MTT assay, L-carnitine inhibited cellular proliferation and induced reactive oxygen species (ROS) in HCT116 by DCF-DA analysis. To analyze the mechanism of L-carnitine in colorectal cancer cells, we performed a western blot analysis for pERK1/2 and pp38 MAP kinase. The western blot showed that L-carnitine significantly increased protein levels of pERK1/2 and pp38 compared with control. Taken together, we found that L-carnitine has anti-proliferative function via increased ROS and activation of ERK1/2 and p38 pathway in HCT116. These findings suggest that L-carnitine may have an anti-proliferative role on colorectal cancer.

• Korean Journal of Food Science and Technology
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• v.36 no.5
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• pp.812-817
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• 2004

Cytotoxic effects of Korean rice-wine (Yakju) made with different processes and ingredients (Korean rice-wines I, II), red wine, white wine, beer, and Japanese rice-wine (Sake) were examined against human cancer lines (DLD-1, HepG2, K562) and mouse cancer lines (EMT6, LLC1). Red wine showed cytotoxic effect on all cancer lines, while Korean rice-wines I, and II showed cytotoxcity on all cancer cells except DLD-1. White wine, beer, and Japanese rice-wine had no or little cytotoxic effect against all cancer cell lines. Concentrate of Korean rice-wine only showed cytotoxic effect against DLD-1. These results suggest Korean rice-wine has strong anti-cancer effects, which are induced by certain rice-wine components.

• Journal of Gastric Cancer
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• v.7 no.2
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• pp.59-66
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• 2007

Purpose: This study was aimed at evaluating the diagnostic validity of peritoneal dissemination of gastric cancer cells by performing multiple genetic marker analysis via quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) in gastric cancer cell lines and gastric cancer tissues. Materials and Methods: Quantitative RT-PCR was performed on 12 human gastric cancer cell lines and 10 gastric cancer tissues with four mRNAs of carcinoembryonic antigen (CEA), Cytokeratin 20 (CK20), dopa decarboxylase (DDC), and L-3-phosphoserine phosphatase (L3PP). Results: Out of the 12 human gastric cancer cell lines we tested, CEA was overexpressed in four cell lines (33%), CK20 in one (8%), DDC in six (50%) and L3PP was expessed in all the lines (100%). Out of the 10 gastric cancer tissues we tested, CEA was overexpressed in nine tissues, CK20 in eight, DOC in nine and L3PP was overexpressed in all the tissues. L3PP was overexpressed in all the gastric cancer cell lines and tissues, but the levels of overexpression were lower than those of CEA and DDC. Conclusion: Multiple genetic marker analysis can compensate for the weak points of single marker analysis when testing gastric cancer, and three mRNAs of CEA, DDC and L3PP can be used as candidate genes.

• Journal of Life Science
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• v.23 no.5
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• pp.689-697
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• 2013

In the United States, about 40,000 new cases of oral cancer are diagnosed each year and nearly 7,800 patients died from it in 2012. Omega-3 polyunsaturated fatty acids have been found to have anticancer effects in a variety of cancer cell lines and animal models, but their effect in oral cancer remains unclear. This study was designed to examine the effect of docosahexaenoic acid (DHA, a kind of omega-3 fatty acid) on oral cancer cells and the molecular mechanism of its action. We found that exposure of squamous cell carcinoma-4 (SCC-4) and squamous cell carcinoma-9 (SCC-9) human oral cancer cells to DHA induced growth inhibition in a dose- and time-dependent manner. Meanwhile, in addition to the elevated levels of apoptotic markers, such as cleaved PARP, subG1 portion and TUNEL-positive nuclei, DHA led to autophagic vesicle formation and an increase in autophagic flux, indicating the involvement of both apoptosis and autophagy in the inhibitory effects of DHA on oral cancer cells. Further experiments revealed that the apoptosis and autophagy induced by DHA were linked to inhibition of mammalian target of rapamycin (mTOR) signaling by AKT inhibition and AMP-activated protein kinase (AMPK) activation in SCC-9 cells. Together, our results suggest that DHA induces apoptosis- and autophagy-associated cell death through the AMPK/AKT/mTOR signaling pathway in oral cancer cells. Thus, utilization of omega-3 fatty acids may represent a promising therapeutic approach for chemoprevention and treatment of human oral cancer.

• Food Engineering Progress
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• v.15 no.1
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• pp.64-69
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• 2011

The anticancer activity of Schizandra chinensis Baillon was investigated for the development of functional food resources. The antiproliferative activity of hot water extracts of Schizandra chinensis Baillon in human colon cancer cell line (HT-29) were identified using cell viability, morphology study, cell cycle and RT-PCR analyses. HT-29 cells were cultured in several concentrations (0, 1.0, 2.0, 4.0 mg/mL) of water extracts of Schizandra chinensis Baillon. In our study, colon cancer cell growth could be inhibited by hot water extracts of Schizandra chinensis Baillon in a dose-dependent manners. It was associated with morphological changes and apoptotic cell death with cell shrinking, chromatin condensation, apoptotic bodies and cell cycle analysis. These results suggest that Schizandra chinensis Baillon may inhibit the growth of human colon cancer cells by various apoptosis-aiding activities as well as apoptosis itself.

• Korean Journal of Food Science and Technology
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• v.32 no.3
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• pp.699-705
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• 2000

The superoxide scavenging activities of thirteen kinds of herbal extracts were examined together with their cytotoxic and immunomodulating effects. The extracts of 6 kinds of herbs such as eucalyptus, mate, peppermint, sage, thyme and yarrow, so called medicinal herbs, showed above 70% of the superoxide scavenging activities. They also showed cytotoxicities against the cancer cell lines of Hepa-1c1c7 and KB-3-1 as well as the normal fibroblast cell line of mouse. The $IC_{50}$ values of above 6 herb extracts on the cancer cell lines were above or similar to the $IC_{50}$ values on the normal cell line, so it was unable to observe the herb extract which showed cytotoxicity only to the cancer cell lines. Considering the results of nitric oxide test that the sage extract was the only one having the immunomodulating effect(37% of positive control), there was no significant relationship between the superoxide scavenging activities of herbs and their immunomodulating effects.

• Journal of Life Science
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• v.16 no.5
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• pp.759-766
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• 2006

Acute promyelocytic leukemia (APL) is a myeloid leukemia caused by over-expression of fusion protein, PML/RAR$({\alpha})$, which was the result of chromosomal translocation and induces the blockage of differentiation of affected promyelocytes. Pharmacological dose of retinoic acid induces the activation of and subsequent degradation of PML/RAR$({\alpha})$ fusion protein, and then APL cells undergo through the normal differentiation pathway. Arsenic trioxide has proved effective in causing remission of acute promyelocytic leukemia by inducing apoptosis of this tumor cells, whereas the heterogeneity of cellular susceptibility to this cytotoxic agent limited its usage on more types of tumors in clinic. This work showed that arsenic trioxide could induce apoptosis of a panel of acute promyelocytic leukemic cell lines, all-trans-retinoic acid (ATRA) sensitive NB4 cells and ATRA resistant UF-1 cell. They were investigated with regard to the correlation between the inherent or intrinsic cellular level of GSH and the apoptotic susceptibility of the cells to arsenic trioxide. We manifested, in two cell types, the inherently existed difference in intracellular GSH level reactive to the arsenic trioxide, and a positive correlation between the GSH level and their apoptotic sensitivity to arsenic trioxide. And it showed that arsenic trioxide could differentiate promyelocytic cancer cells to the cells possessed of dendritic cell surface markers. Unravelling the cause of the different susceptibility between leukemic cells and proving that promyelocyte could be differentiated to dendritic cells by arsenic trioxide will help not only to understand the mechanism underlying the complete remission of acute promyelocytic leukemia induced by arsenic trioxide, but also to expand its clinical usage.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.9
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• pp.1451-1456
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• 2004

Amino acid transporters play an important role in supplying nutrients to normal and cancer cells for cell proliferation. System L is a major transport system responsible for the $Na^+$ -independent, large neutral amino acids including several essential amino acids. L-type amino acid transporter 1 (LAT1), an isoform of system L amino acid transporter, is highly expressed presumably to support their continuous growth and proliferation in malignant tumors. In the present study, we have examined the correlation between the expressions of amino acid transporter LAT1 mRNA and its subunit 4F2hc mRNA and the amount of L-leucine transport in various human cancer cell lines. Northern blot analysis have revealed that the 26 human cancer cell lines expressed LAT1 mRNA and 4F2hc mRNA. There were the differences for the levels of LAT1 and 4F2hc mRNA expressions in the 26 human cancer cell lines. The 26 human cancer cell lines transported the L-[$^{14}C$]leucine into the cells via amino acid transporter. In the 26 human cancer cell lines, a linear relationship was observed between the expression of amino acid transporter LAT1 mRNA and the amount of L-leucine transport. Little relationship was observed between the expression of 4F2hc mRNA and the amount of L-leucine transport, but the statistical significance of difference was not detected. These results indicate that the 26 human cancer cell lines express LAT1 mRNA and 4F2hc mRNA and there is the correlation between the expression of amino acid transporter LAT1 mRNA and the amount of L-leucine transport. In addition, specific inhibition of LAT1 in cancer cells will be a new rationale for anti-cancer therapy.

• Journal of Life Science
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• v.32 no.4
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• pp.271-278
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• 2022

The detailed mechanism by which cancer upregulated gene 2 (CUG2) overexpression induces cancer stem cell-like phenotypes is not fully understood. The downregulation of FBXW7 E3 ligase, a tumor suppressor known for its proteolytic regulation of oncogenic proteins such as cyclin E, c-Myc, Notch, and Yap1, has been frequently reported in several types of tumor tissues, including those in the large intestine, cervix, and stomach. Therefore, we investigated whether FBXW7 is involved in CUG2-induced oncogenesis. In this study, the decreased expression of FBXW7 was examined in human lung adenocarcinoma A549 (A549-CUG2) and human bronchial BEAS-2B cells (BEAS-CUG2) overexpressing CUG2 and compared with control cells stably expressing an empty vector (A549-Vec or BEAS-Vec). Treatment with MG132 (a proteosome inhibitor) prevented the degradation of FBXW7 and Yap1 proteins, which are substrates of the FBXW7 E3 ligase. To address the role of Fbxw7 in the development of cancer stem cell (CSC) phenotypes, we suppressed Fbxw7 protein levels using its siRNA. We observed that decreased levels of FBXW7 enhanced cell migration, invasion, and spheroid size and number in A549-Vec and BEAS-Vec cells. The enforced expression of FBXW7 produced the opposite results in A549-CUG2 and BEAS-CUG2 cells. Furthermore, the downregulation of FBXW7 elevated the activities of EGFR, Akt, and ERK1/2 and upregulated β-catenin, Yap1, and NEK2, while the enforced expression of FBXW7 generated the opposite results. We thus propose that FBXW7 downregulation induced by CUG2 confers CSC-like phenotypes through the upregulation of both the EGFR-ERK1/2 and β-catenin-Yap1-NEK2 signaling pathways.