• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.86-86
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• 2003

In a continuous effort to develop novel anticancer agents we newly synthesized and evaluated the antitumor activity of nucleoside analogues. One analogue, 4 - ［2-Chlor-6- (3-iodo- benzy lamino) -purin -9-yl］- 2,3-dihydroxy-cyclopentanecarbo xylic acid methylamide (LJ-331), has been shown to exert a potent inhibition of human cancer cell growth in vitro including human lung (A549), stomach (SNU-638) and leukemia (HL-60) cancer cells. Following mechanism of action study revealed that LJ - 331induces cell cycle arrest at the G1 phase in HL-60 cells and evokes apoptotic phenomena such as an increase in DNA ladder intensity and chromatin condensation by a dose- and time-dependent manner. LJ-331 also activated the caspase-3 activity in HL-60. This result suggests that the growth inhibition of human cancer cells by LJ-331 might be related to the cell cycle arrest and induction of apoptosis.

• Tuberculosis and Respiratory Diseases
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• v.77 no.3
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• pp.111-115
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• 2014

Lung cancer is the leading cause of cancer-related mortality worldwide, and more than 80% of cases are of non-small cell lung cancer. Although chemotherapy and molecularly targeted therapy may provide some benefit, there is a need for newer therapies for the treatment of patients with advanced NSCLC. Immunotherapy aims to augment the recognition of cancer as foreign, to stimulate immune responsiveness, and to relieve the inhibition of the immune response that allows tolerance to tumor survival and growth. Two immunotherapeutic approaches showing promise in NSCLC are immune checkpoint inhibition and cancer vaccination. Although currently immunotherapy does not have an established role in the treatment of NSCLC, these patients should be enrolled in formal clinical trials.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.1
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• pp.205-209
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• 2012

Background: The inhibition of tumor cell growth without toxicity to normal cells is an important target in cancer therapy. One possible way to increase the efficacy of anticancer drugs and to decrease toxicity or side effects is to develop traditional natural products, especially from medicinal plants. Paris polyphylla Smith has shown anti-tumour effects by inhibition of tumor promotion and inducement of tumor cell apoptosis, but mechanisms are still not well understood. The present study was to explore the effect of Paris polyphylla Smith extract (PPSE) on connexin26 and growth control in human esophageal cancer ECA109 cells. Methods: The effects of PPSE on Connexin26 were examined by RT-PCR, western blot and immunofluorescence; cell growth and proliferation were examined by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay. Results: PPSE inhibited the growth and proliferation on esophageal cancer ECA109 cells, while increasing the expression of connexin26 mRNA and protein; conversely, PPSE decreased Bcl-2 and increased Bad. Conclusion: This study firstly shows that PPSE can increase connexin26 expression at mRNA and protein level, exerting anti-tumour effects on esophageal cacner ECA109 cells via inhibiting cell proliferation and inducing cell apoptosis.

• Environmental Analysis Health and Toxicology
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• v.27
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• pp.10.1-10.7
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• 2012

Objectives: In recent years, a number of structurally diverse Histone deacetylase (HDAC) inhibitors have been identified and these HDAC inhibitors induce growth arrest, differentiation and/or apoptosis of cancer cells in vitro and in vivo. This study aimed at investigating the antitumor activity of newly synthesized HDAC inhibitor, 3-(4-dimethylamino phenyl)-N-hydroxy-2-propenamide (IN-2001) using human breast cancer cells. Methods: We have synthesized a new HDAC inhibitor, IN-2001, and cell proliferation inhibition assay with this chemical in estrogen receptor-positive human breast cancer MCF-7 cells. Cell cycle analysis on MCF-7 cells treated with IN-2001 was carried out by flow cytometry and gene expression was measured by RT-PCR. Results: In MCF-7 cells IN-2001 showed remarkable anti-proliferative effects in a dose- and time-dependent manner. In MCF-7 cells, IN-2001 showed a more potent growth inhibitory effect than that of suberoylanilide hydroxamic acid. These growth inhibitory effects were related to the cell cycle arrest and induction of apoptosis. IN-2001 showed accumulation of cells at $G_2$/M phase and of the sub-$G_1$ population in a time-dependent manner, representing apoptotic cells. IN-2001-mediated cell cycle arrest was associated with HDAC inhibitor-mediated induction of CDK inhibitor expression. In MCF-7 cells, IN-2001 significantly increased $p21^{WAF1}$ expression. Conclusions: In summary, cyclin-dependent kinase (CDK) induced growth inhibition, possibly through modulation of cell cycle and apoptosis regulatory proteins, such as CDK inhibitors, and cyclins. Taken together, these results provide an insight into the utility of HDAC inhibitors as a novel chemotherapeutic regime for hormone-sensitive and insensitive breast cancer.

• Journal of Microbiology and Biotechnology
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• v.21 no.5
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• pp.477-482
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• 2011

There are accumulating evidences suggesting that connexin (Cx), a gap junction channel-forming protein, acts as a growth suppressor in various cancer cells, and this effect is attributeed to the gap junction-mediated intercellular communication (GJIC). In order to characterize the relationship between the growth-arresting activity of Cx26 and its cytoplasmic localizations after expression, we linked a nuclear export signal (NES) sequence to Cx26 cDNA before transfecting into a rat breast cancer cell line. A confocal fluorescent microscopic observation revealed that the insertion of NES minimized the nuclear expression of Cx26, and increased its cytoplasmic expression, including plasma membrane junctions. Total cell counting and BrdUrd-labeling experiments showed that the growth of the breast cancer cells was inhibited by 74% upon transfection of Cx26-NES, whereas only 9% inhibition was observed with only Cx26 cDNA.

• Korean Journal of Environmental Biology
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• v.28 no.4
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• pp.196-201
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• 2010

The phenethyl ester of caffeic acid (CAPE), an active component of honeybee propolis extract, is shown to inhibit cancer growth previously. However, studies on human ovarian cancer are largely obscure. This study evaluated the effects of CAPE as a potential anti-proliferative and pro-apoptotic agent in the human ovarian cancer line, OVCAR-3. CAPE treated OVCAR-3 cells showed inhibition of cell viability and proliferation in a dose-dependent manner by WST-1 assay, LDH assay and bromodeoxyuridine (BrdU) incorporation assay. Furthermore, CAPE-mediated OVCAR-3 cell growth inhibition was associated with apoptotic changes as evident by cell cycle arrest and accumulation of cells in the apoptotic phase and DNA fragmentation. Taken together, CAPE inhibits cell proliferation via DNA synthesis reduction and induces apoptotic cell death via DNA damage, thus elucidating a novel, plausible mechanism of CAPE anti-tumorigenic property in OVCAR-3 cells.

• Advances in Traditional Medicine
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• v.1 no.2
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• pp.1-5
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• 2000

• Journal of Ginseng Research
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• v.17 no.3
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• pp.196-202
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• 1993

A study was performed to compare the anticancer effects of Korean and Chinese red ginseng roots. The whole crude extracts or chloroform, methanol and acetone fractions of the crude extracts were added in the culture medium of three cancer cell lines, a mouse leukemia cell line ($P_{388}$), a human colon carcinoma cell line (HT-29) and a human rectal carcinoma cell line (HRT-18), to screen the growth inhibition effects. The results are summarized as follows : 1. Crude extracts of both Korean and Chinese red ginseng roots inhibited the proliferation of all the three cancer cell lines tested in a dose dependent manner. However, the growth inhibition effects of Korean red ginseng extracts were significantly greater than that of Chinese red ginseng. 2. An acetone fraction showed the greatest antiproliferative effects among the 11'hole crude extracts, chloroform, methanol and acetone fractions of the crude extracts. 3. These results suggest that the active antiproliferative components of the crude extracts are present mostly in the acetone fraction.

• YAKHAK HOEJI
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• v.38 no.5
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• pp.579-585
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• 1994

Antitumor activity was tested by administration of reaction mixture of green onion extract and chitin to mice bearing sarcoma-180 cells. An intraperitoneal injection of mixture(20 mg/kg/day) to mice Have an 52% inhibition of tumor growth. Inhibition of tumor growth was found to be dose-dependent. When eighty miligrams of the mixture were administered, the weight of tumor was reduced significantly. HPLC analysis indicated the mixture was composed of N-acetyl-D-glucosamine, N-acetylchitobiose and N-acetylchitotriose.

• Korean Journal of Food Science and Technology
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• v.38 no.2
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• pp.262-267
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• 2006

Inhibitory effects of fungal metabolites isolated from foodstuffs on growth of human cancer cell lines were evaluated. Isolated strains were divided into four classes based on color (aerial, reverse), shape, and growth speed. Fungal metabolites extracted with ethyl acetate were investigated for their growth inhibition on six kinds of human cancer cells by MTT assay. Ethyl acetate extract showed high growth inhibition against all cancer cells tested, with D4 exhibiting the strongest growth inhibition effects against Kato III, AGS, Hepa1c1c7, and MDA-MB-231 cancer cells. These results suggest ethyl acetate extract from fungal metabolites as effective natural cancer therapeutic material.