• Journal of Acupuncture Research
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• v.32 no.1
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• pp.79-88
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• 2015

Objectives : The purpose of this research was to investigate the cytotoxic effect of Natural Killer(NK)-92 cell and Snake Venom, and to elucidate its mechanism on human lung carcinoma cell A549. Methods : In order to figure out whether Snake Venom enhances the cytotoxic effect of NK-92 cell in A549 cell, Cell Viability Assay was conducted. Also, in order to observe the changes of Caspase-3 and Caspase-8, both of which are proteinases that advance apoptosis, and the changes of TNRF and DR3, which are Death Receptors of the extrinsic pathway of apoptosis, Western Blot Analysis was conducted. By conducting RT-PCR analysis, we have tried to confirm Perforin, Granzyme B, and GADPH, all of which are cytotoxic-related proteins. Lastly, in order to observe the effect of Snake Venom on NO formation within human lung carcinoma cells, NO determination was conducted. Results : 1. After conducting Cell Viability Assay, Snake Venom enhanced the cytotoxic effect of NK-92 cell and inhibited the growth of A549. 2. Western Blot Analysis caused proteinases Caspase-3 and Caspase-8, which advance apoptosis, to increase in the combined treatment group, but not in treatment groups that focused only on either Snake Venom or NK-92 cell in A549 lung carcinoma cells. 3. Western Blot Analysis caused an expression of TNFR2 and DR3, both of which are Death Receptors of the apoptosis extrinsic pathway, in the combined treatment group, but not intreatment groups that focused only on either Snake Venom or NK-92 cell in A549 human lung carcinoma cells. 4. After conducting NO determination, NO formation within A549 cell showed no significant changes in both treatment groups that focused NK-92 cell and combined treatment group. 5. After conducting RT-PCR, the expression of Granzyme B and Perforin, which are cytotoxic-related proteins within A549 human lung carcinoma cells, showed growth in the combined treatment group, but not the treatment group that focused only on NK-92 cell. Conclusion : It has been indicated that, when it comes to the A549 cell, Snake Venom enhances the increase of Death Receptor expression and continuous apoptosis reaction, leading to the enhancement of the cancer cell cytotoxic effect of the NK-92 cell. It is expected that Snake Venom can be used with the NK-92 cell for further lung cancer treatment.

• Food Science of Animal Resources
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• v.22 no.4
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• pp.348-351
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• 2002

This study was carried out to investigate the anticancer effect of extracts from sulfur fed duck carcass. Growth inhibition of cancer cell lines was measured by MTT assay. Eleven cancer cell lines, such as Calu-3(human lung carcinoma), SK-MES-1(human lung carcinoma), HL6O(human leukemia), KB(human epidermoid of mouth carcinoma), Farrow(human melanoma), HEP-2(human larynx carcinoma), SNU-1(human stomach carcinoma), K-562 (human leukemia), WiDr(human colon carcinoma), P388(mouse leukemia) and 3LL(mouse lung carcinoma) showed the growth inhibition higher than 50%, but those, such as SF-188(human brain carcinoma), A-549(human lung carcinoma) and HEC-lB(human uterus carcinoma) showed the growth inhibition lower than 50% in the extract of sulfur fed duck carcass at the concentration of 10 mg/㎖. The sulfur fed duck carcass extract had better growth inhibition than the normal counterpart against various cancer cell lines at the concentration of 10 mg/㎖. When the effect of growth inhibition of an effluent by different concentrations of methyl alcohol(25, 50, 75 and 100%) tested on Diaion HP-20 column chromatography, an effluent by concentration of 100% methyl alcohol showed the most strong effect of growth inhibition against HEP-2(human larynx carcinoma).

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.17
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• pp.7467-7471
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• 2014

SCY1-like 1-binding protein 1 (SCYL1BP1) is a newly identified transcriptional activator domain containing protein with many unknown biological functions. Recently emerging evidence has revealed that it is a novel regulator of the p53 pathway, which is very important for the development of human cancer. However, the effects of SCYL1BP1 on human lung squamous carcinoma cell biological behavior remain poorly understood. In this study, we present evidence that SCYL1BP1 can promote the degradation of MDM2 protein and further inhibit the G1/S transition of lung squamous carcinoma cell lines. Functional assays found that reintroduction of SCYL1BP1 into lung squamous carcinoma cell lines significantly inhibited cell proliferation, migration, invasion and tumor formation in nude mice, suggesting strong tumor suppressive function of SCYL1BP1 in lung squamous carcinoma. Taken together, our data suggest that the interaction of SCYL1BP1/MDM2 could accelerate MDM2 degradation, and may function as an important tumor suppressor in lung squamous carcinomas.

• Journal of Pharmacopuncture
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• v.13 no.1
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• pp.5-14
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• 2010

Objectives : This study was performed to examine the anticancer effect of mountain ginseng Pharmacopuncture(MGP) to the nude mouse of lung carcinoma induced by NCI-H460 human nonsmall lung cancer cells. Methods : Human lung cancer (NCI-H460) cells were cultured and applied to evaluate anti-tumor activity in nude mice. After confirmed tumor growth in mice, MGP was treated per 0.1ml/kg dose to intraperitoneal and intravenous injection everyday for four weeks. And checked the changes in body weights, tumor volume, mean survival time and percent, increase in life span, histo-pathological findings, organ weights, and blood chemistry levels. Results : The results of in vivo study showed that MGP may have potential as growth inhibitor of solid tumor induced NCI-H460 without marked side effects. MGP inhibited dosage-dependently the growth of NCI-H460 cell-transplanted solid tumor compared with the control group. And mean survival time of MGP treated group was prolonged comparing with control group. Generally the group of intravenous injection is more effective than intraperitoneal injection. Conclusion : These results were suggested that MGP may be a useful anticancer agent for therapy of human lung cancer. And follow study need for the certain evidence.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1102-1106
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• 2004

To investigate the anti-proliferative effects of an aqueous extract of Cordyceps militaris (AECM) on the growth of human lung carcinoma cell line A549, we performed various biochemical experiments such as the effects of AECM on the cell proliferation and viability, the morphological changes, the effects on expression of apoptosis and cell growth-regulatory gene products. Results obtained are as follow; AECM treatment declined the cell viability and proliferation of A549 cells in a concentration-dependent manner. The anti-proliferative effect by AECM treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. Taken together, these findings suggest that AECM-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products, and C. militaris may have therapeutic potential in human lung cancer.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.150.2-151
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• 2003

We have focused on various biological activities of acharan sulfate (AS) isolated from the giant African snail Achatina fulica. In a previous study, AS showed antiangiogenic and immunomodulating activity. We also investigated antitumor activity of AS. In vitro AS had no cytotoxicity within 0 to 200 ug/ml in tumor cells such as Lewis lung carcinoma(LLC) , KM1214 (human colon cancer cell) and Caki-1 (human kidney cancer cell) by both MTT and SRB assay. In vivo AS was used to treat C57BL/6 mice bearing LLC by subscutaneous injection. (omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7295-7300
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• 2013

Lung cancer is the most common cause of cancer-related death in the world. The main types are small-cell lung carcinoma (SCLC) and non-small-cell lung carcinoma (NSCLC), the latter including squamous cell carcinoma (SCC), adenocarcinoma and large cell carcinoma. NSCLCs account for about 80% of all lung cancer cases. Microcephalin (MCPH1), also called BRIT1 (BRCT-repeat inhibitor of hTERT expression), plays an important role in the maintenance of genomic stability. Recently, several studies have provided evidence that the expression of MCPH1 gene is decreased in several different types of human cancers. We evaluated the expression of protein MCPH1 in 188 lung cancer and 20 normal lung tissues by immunohistochemistry. Positive MCPH1 staining was found in all normal lung samples and only some cancerous tissues. MCPH1-positive cells were significantly lower in lung carcinoma compared with normal tissues. Furthermore, we firstly found that MCPH1 expression in lung adenocarcinoma is higher than its expression in squamous cell carcinoma. Change in MCPH1 protein expression may be associated with lung tumorigenesis and may be a useful biomarker for identification of pathological types of lung cancer.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1147-1152
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• 2004

To investigate the anti-cancer effects of aqueous extract of Cheonkumwikyung-tang (CKWKT) on the growth of human lung carcinoma cell line A549, we performed various biochemical experiments such as the effects of CKWKT on the cell proliferation and viability, the morphological changes, the effects on expression of apoptosis and cell growth-regulatory gene products. Results obtained are as follow; CKWKT treatment declined the cell viability and proliferation of A549 cells in a concentration-dependent manner. The anti-proliferative effect by CKWKT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CKWKT treatment induced apoptotic cell death of A549 cells in a concentration-dependent manner, which was associated with inhibition and/or degradation of apoptotic target proteins such poly(ADP-ribose) polymerase, β-catenin and phospholipase C-γ1. Western blot analysis revealed that the levels cyclin-dependent kinase inhibitor p21 expression were induced by CKWKT treatment in A549 cells. Taken together, these findings suggest that CKWKT-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products and CKWKT may have therapeutic potential in human lung cancer.

• Biomedical Science Letters
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• v.10 no.3
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• pp.195-202
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• 2004

Lung cancer is a leading cause of cancer death worldwide; however, despite major advances in cancer treatment during the past two decades, the prognostic outcome of lung cancer patients has improved only minimally. This is largely due to the inadequacy of the traditional screening approach of diagnosis in lung cancer, which detects only well­established overt cancers and fails to identify precursor lesions in premalignant conditions of the bronchial tree. In recent years this situation has fundamentally changed with the identification of molecular abnormalities characteristic of premalignant changes; these concern tumour suppressor genes, loss of heterozygosity at crucial sites and activation of oncogenes. Basic knowledge at the molecular level has extremely important clinical implications with regard to early diagnosis, risk assessment and prevention, and therapeutic targets. In this study we used a 'cap-finder' subtractive hybridization method, 'long distance' polymerase chain reaction (PCR), streptavidin magnetic beads mediated subtraction, and spin column chromatography to detect differential expression genes of human small cell lung carcinoma. We have now isolated ninety two genes that expressed differentially in the human small cell lung carcinoma cells and analyzed of 12 clones with sequencing, nine cDNAs include tapasin (NGS-17) mRNA, BC200 alpha scRNA, chromosome 12q24 PAC RPCI3-462E2, protein phosphatase 1 (PPPICA), translocation protein 1 (TLOC1), ribosomal protein S24 (RPS24) mRNA, protein phosphatase (PPEF2), cathepsin Z, MDM2 gene and three novel genes. They may be oncogenesis­related proteins.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3751-3755
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• 2012

Aim: Tea polyphenols are known to play roles in critical steps of human lung carcinoma cell metastasis. For understanding the mechanisms whereby they inhibit tumor metastasis, the present study was conducted to investigate their effects on the adhesion of highly metastatic lung carcinoma cell lines (PG cells) to endothelial cells (EC cells) and adhesion molecule expression in vitro. Methods: The expression of CD44 or CD54 in the PG cells was detected by flow cytometry and adhesion of PG cells to EC cells was assessed by confocal microscopy double fluorescence staining. Results: The results showed that tea polyphenols: (1) inhibited the expression of CD44 and CD54, two important adhesion molecules in the PG cells in a dose-dependent manner; (2) significantly blocked the adhesion of PG cells to EC cells not only in a state of rest but also when active; and (3) influenced CD44 and CD54 expression during the adhesion process of PG cells to EC cells. Conclusions: The data indicated that the blocking role of tea polyphenols in the adhesion of PG cells to EC cells is related to CD44 and CD54. The mechanism of tea polyphenol prevention of human lung carcinoma metastasis might be through inhibiting adhesion molecule expression to block cancer cell adhesion.