• The Korean Journal of Physiology and Pharmacology
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• v.18 no.1
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• pp.61-66
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• 2014

Lung cancer is still the number one cause of death from cancer worldwide. The clinical effect of platinum-based chemotherapy for non-small cell lung cancer is constrained by the resistance to drug. To overcome chemo-resistance, various modified treatment including combination therapy has been used, but overall survival has not been improved yet. In this study, chemo-resistant lung cancer cells, A549/Cis and H460/Cis, were developed by long-term exposure of cells to cisplatin and the proliferative capability of these resistant cells was verified to be reduced. We found cytotoxic effect of epigallocatechin gallate (EGCG), a major catechin derived from green tea, on both the parental lung cancer cells, A549 and H460, and their cisplatin resistant cells, A549/Cis and H460/Cis. ELISA and Western blot analysis revealed that EGCG was able to increase interlukine-6 (IL-6) production per cell, whereas its downstream effector Signal transducers and activators of transcription 3 (STAT3) phosphorylation was not changed by EGCG, indicating that IL-6/STAT3 axis is not the critical signaling to be inhibited by EGCG. We next found that EGCG suppresses the expression of both Axl and Tyro 3 receptor tyrosine kinases at mRNA and protein level, explaining the cytotoxic effect of EGCG on lung cancer cells, especially, regardless of cisplatin resistance. Taken together, these data suggest that EGCG impedes proliferation of lung cancer cells including their chemo-resistant variants through downregulation of Axl and Tyro 3 expression.

• Journal of Ginseng Research
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• v.46 no.5
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• pp.690-699
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• 2022

Background: Few studies reported the therapeutic effect of Korean Red Ginseng (KRG) in lung inflammatory diseases. However, the anti-inflammatory role and underlying molecular in cadmium-induced lung injury have been poorly understood, directly linked to chronic lung diseases (CLDs): chronic obstructive pulmonary disease (COPD), cancer etc. Therefore, in this study we aim to investigate the therapeutic activities of water extract of KRG (KRG-WE) in mouse cadmium-induced lung injury model. Method: The anti-inflammatory roles and underlying mechanisms of KRG-WE were evaluated in vitro under cadmium-stimulated lung epithelial cells (A549) and HEK293T cell line and in vivo in cadmium-induced lung injury mouse model using semi-quantitative polymerase chain reaction (RT-PCR), quantitative real-time PCR (qPCR), luciferase assay, immunoblotting, and FACS. Results: KRG-WE strongly ameliorated the symptoms of CdSO4-induced lung injury in mice according to total cell number in bronchoalveolar lavage fluid (BALF) and severity scores as well as cytokine levels. KRG-WE significantly suppressed the upregulation of inflammatory signaling comprising mitogen-activated protein kinases (MAPK) and their upstream enzymes. In in vitro study, KRG-WE suppressed expression of interleukin (IL)-6, matrix metalloproteinase (MMP)-2, and IL-8 while promoting recovery in CdSO₄-treated A549 cells. Similarly, KRG-WE reduced phosphorylation of MAPK and c-Jun/c-Fos in cadmium-exposed A549 cells. Conclusion: KRG-WE was found to attenuate symptoms of cadmium-induced lung injury and reduce the expression of inflammatory genes by suppression of MAPK/AP-1-mediated pathway.

• BMB Reports
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• v.49 no.11
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• pp.623-628
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• 2016

GPR78 is an orphan G-protein coupled receptor (GPCR) that is predominantly expressed in human brain tissues. Currently, the function of GPR78 is unknown. This study revealed that GPR78 was expressed in lung cancer cells and functioned as a novel regulator of lung cancer cell migration and metastasis. We found that knockdown of GPR78 in lung cancer cells suppressed cell migration. Moreover, GPR78 modulated the formation of actin stress fibers in A549 cells, in a RhoA- and Rac1-dependent manner. At the molecular level, GPR78 regulated cell motility through the activation of $G{\alpha}q$-RhoA/Rac1 pathway. We further demonstrated that in vivo, the knockdown of GPR78 inhibited lung cancer cell metastasis. These findings suggest that GPR78 is a novel regulator for lung cancer metastasis and may serve as a potential drug target against metastatic human lung cancer.

• Journal of Haehwa Medicine
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• v.9 no.1
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• pp.155-167
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• 2000

To evaluate the antitumor activity and antimetastatic effects of Gobongeerlhobang(GG1B), studies were done experimentally. The results were obtained as follows: 1. GG1B extracts exhibited a significant cytotoxicity against HT1080, A549, SK-MEL-2 and SK-OV-3 cell lines. 2. The T/C% was 120.7% in GG1B treated group in S-180 bearing ICR mice. 3. GG1B extracts exhibited inefficient adhesive effect of A549, B16-BL6 cell to complex extracellular matrix. 4. GG1B extracts showed a significant inhibition of lung metastasis of B16-BL6 cells in C57BL/6. 5. In CAM assays, angiogenesis was insignificantly inhibited in GG1B treated group than control group. These results suggested that GG1B extracts might be usefully applied for prevention and treatment of cancer.

• Journal of Physiology & Pathology in Korean Medicine
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• v.34 no.4
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• pp.170-176
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• 2020

Palmijihwang-tang is an herbal formula frequently used to treat many symptoms, such as lumbago, pollakiuria, cold hands and feet, nephritis, sterilitas virilis, and prostatic disorders. The aim of this study was to investigate the effects of Palmijihwang-tang on cisplatin-induced nephrotoxicity in rat kidney proximal tubular NRK-52E cells. NRK-52E cells were treated with Palmijihwang-tang in absence or presence of 30 µM cisplatin for 12 or 24 h. Palmijihwang-tang at concentrations of 50-800 ㎍/ml did not change the cell viability in NRK-52E cells, and showed no significant toxicity. Palmijihwang-tang at concentrations of 400 and 800 ㎍/ml significantly increased the cell viability and reduced apoptotic cells in NRK-52E cells exposed to cisplatin. Also, Palmijihwang-tang markedly inhibited cisplatin-induced caspase-3 activation, PARP cleavage, ROS production and p53 activation in NRK-52E cells. Furthermore, Palmijihwang-tang did not interfere with the antitumor activity of cisplatin in AGS and A549 cancer cells. Particularly, Palmijihwang-tang enhanced antitumor activity of cisplatin in A549 cells. Taken together, these results suggest that Palmijihwang-tang ameliorated cisplatin-induced nephrotoxicity through reduction of ROS production and p53 activation, and did not interrupt antitumor efficacy of cisplatin against cancer cells.

• 한국생물공학회:학술대회논문집
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• 2002.04a
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• pp.581-584
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• 2002

Individual surface(hydrophilic/hydrophobic) were prepared and mammalian cells were cultured on the hydrophilic region. For drug test, cancer and normal cells were treated with Taxol, as an example. Our system was compared with MTT assay. CHO cells were resistant to Taxol up to 100 nM in both Methods. However, A549 cells was sensitive at 100 nM Taxol in the 2 day-treatment. Cervical carcinoma cell, HeLa, was very sensitive to Taxol. In our system, the cells were not shown from above 20 nM Taxol treatment. Our system was competitive to MTT assay in animal cells for drug test.

• Journal of Life Science
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• v.34 no.6
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• pp.365-376
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• 2024

The present study assessed the cytotoxic effects on cell growth and senescence in human cancer (A-549, AGS, HCT-116, MDA-MB-231, and U 87-MG) and normal (MRC-5 and mesenchymal stem cells) cell lines treated with efavirenz (EFA), an inhibitor of non-nucleoside reverse transcriptase (RTase). Following EFA treatment, the half-maximal inhibitory concentration (IC₅₀) values were approximately 15 µM, and the IC₅₀ value was significantly (p<0.05) lower in the cancer cell lines, compared to normal cell lines. After determining the IC₅₀ values against EFA, each cell line was treated with 15 µM EFA for up to one week. Significant (p<0.05) decreases in endogenous RTase and telomerase activity were observed in the cancer cell lines. RTase and telomerase activity were absent or detected at very low levels in both EFA-untreated and treated MRC-5 and MSC normal cells. The cell doubling time (CDT) was also significantly (p<0.05) prolonged by the decreased cell growth rate in the EFA-treated cancer cell lines compared to the untreated cell lines. Furthermore, EFA-treated cancer cells displayed a high number of cells with a high intensity of senescence-associated ß-galactosidase activity (SA-ß-gal activity), compared to the untreated cells. The present study showed that inhibition of RTase activity induces cellular senescence and arrests cell growth in human cancer cell lines; however, normal cell lines showed greater tolerance against EFA. RTase treatment could offer optional chemotherapy for cancer treatment in human cancer cell lines with high RTase activity.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.210.2-210.2
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• 2003

Cornis fructus were extracted by successive extractions and then fractionated with chloroform extract to get active fractions. This study was performed to determine the cytotoxic effect of chloroform extract from Cornis fructus on NIH 3T3 fibroblasts and cancer cell lines using MTT assay. All extracts did not exhibit cytotoxicity in HIH 3T3 fibroblasts. Chloroform extract exhibited antitumor activity in A549, MDA-MB-123, B16 melanoma and SNU-C4 cells. Futher fractionation with chloroform extract was performed to obtain effective fractions. (omitted)

• Journal of Haehwa Medicine
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• v.8 no.2
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• pp.93-106
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• 2000

To evaluate the antitumor activity and antimetastatic effects of Kamicheungyeolhaedog tang(KCHT), studies were done experimentally. The results were obtained as follows: 1. KCHT extracts exhibited a significant cytotoxicity against A549, SK-MEL-2, SK-OV-3, and B16-BL6 cell lines. 2. KCHT extracts showed significant inhibitoty effect on DNA topoisomerase I 3. The T/C% was 145.8% in KCHT treated group in S-180 bearing ICR mice. 4. KCHT extracts exhibited efficient affect adhesive effect of A549, B16-BL6 cell to complex extracellular matrix. 5. In vitro neovascularization assays, angiogenesis was insignificantly inhibited in KCHT treated group as compared with control group. These results suggested that KCHT extracts might be usefully applied for prevention and treatement of cancer.

• Natural Product Sciences
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• v.17 no.2
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• pp.85-89
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• 2011

Bioassay-guided fractionation of the $CHCl_3$-soluble fraction of a MeOH extract of the fruiting bodies of Hygrophorus russula led to the isolation of five ergosterol derivatives (1 - 5). The structures of these compounds were identified as ergosterol peroxide (1), ergosta-4,6,8(14),22-tetraen-3-one (2), ergosta-7,22-diene-3${\beta}$,5${\alpha}$,6${\alpha}$-triol (3), ergosta-7,22-diene-3${\beta}$,5${\alpha}$,6${\beta}$,9${\alpha}$-tetraol (4), and 5${\alpha}$,6${\alpha}$-epoxy-ergosta-8(14),22-diene-3${\beta}$,7${\alpha}$-diol (5) by comparing their physicochemical and spectral data with those in the literature. These compounds were evaluated for in vitro cytotoxicity against A549 and XF498 cancer cell lines. Most of the tested compounds, except for compound 3, exhibited moderate cytotoxicity against both A549 and XF498 cell lines with $IC_{50}$ values ranging from 10.2 to 18.3 ${\mu}g/ml$ and from 11.4 to 24.6 ${\mu}g/ml$, respectively.