• Genomics & Informatics
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• v.12 no.4
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• pp.247-253
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• 2014

Osteosarcoma is the most common primary bone tumor, generally affecting young people. While the etiology of osteosarcoma has been largely unknown, recent studies have suggested that cyclooxygenase-2 (COX-2) plays a critical role in the proliferation, migration, and invasion of osteosarcoma cells. To understand the mechanism of action of COX-2 in the pathogenesis of osteosarcoma, we compared gene expression patterns between three stable COX-2-overexpressing cell lines and three control cell lines derived from U2OS human osteosarcoma cells. The data showed that 56 genes were upregulated, whereas 20 genes were downregulated, in COX-2-overexpressed cell lines, with an average fold-change > 1.5. Among the upregulated genes, COL1A1, COL5A2, FBN1, HOXD10, RUNX2, and TRAPPC2 are involved in bone and skeletal system development, while DDR2, RAC2, RUNX2, and TSPAN31 are involved in the positive regulation of cell proliferation. Among the downregulated genes, HIST1H1D, HIST1H2AI, HIST1H3H, and HIST1H4C are involved in nucleosome assembly and DNA packaging. These results may provide useful information to elucidate the molecular mechanism of the COX-2-mediated malignant phenotype in osteosarcoma.

• Journal of Chest Surgery
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• v.31 no.12
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• pp.1134-1146
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• 1998

Background: The tumor suppressor gene p53 is one of the most frequently altered genes in human tumors, including those of the lung. There is now a compelling evidence that wild-type p53 can negatively influence cell growth by causing G1 arrest or by inducing apoptosis. The possibilities of using p53 for gene therapy are also gathering much interest. Material and Method: Our approach towards understanding p53 function would be to study the biological consequences of overexpression of wild-type p53 in normal and tumor cells by using adenovirus vectors capable of giving high levels of the p53 gene product in cells. We have used this vector containing wild-type p53 to infect tumor cells with different p53 status (null, mutant, or wild-type) to confirm that expression of p53 in null or mutant cell lines becomes possible by Adenovirus-p53 transduction, to examine the effects of high levels of p53 expression on the growth properties of tumor cells, to evaluate the role of apoptosis in p53-mediated biological effects, and to examine the effect of Adenovirus-p53 on the tumorigenicities of the lung cancer cell lines in vitro. Result: The results of our study showed that cells expressing endogenous mutant p53 and those devoid of p53 expression altogether were significantly more sensitive to Adenovirus-p53-mediated cytotoxicity compared to tumor cells expressing endogenous wild-type p53 and that overexpression of wild-type p53 induced programmed cell death. Also we knew that Adenovirus-p53 significantly reduced tumor colony formation of human non-small cell lung cancer cell lines, and decreased the growth of pre-formed colonies in vitro. Conclusion: These results suggest that adenovirus is an efficient vector for mediating transfer and expression of tumor suppressor genes in human non-small cell lung cancer cells and that the tumor cells null for p53 or expressing mutant p53 readily undergo apoptosis by Adenovirus-p53.

• YAKHAK HOEJI
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• v.38 no.1
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• pp.31-37
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• 1994

Active fraction, $P_2$, was Isolated from natural anti-cancer drug, $CP_2$, by HPLC. We confirmed that $P_2$ includes most of the Isoguanosine and minor components, Berberine and other protoberberine alkaloids, by $^1H-NMR$ and $^{13}C-NMR$ and measured tile cytotoxicity of $P_2$ against various tumor cell-lines.' $P_2$ was very effective to all tumor cell-lines, especially to human colon cancer SNU-C2A$(ED_{50};\;24{\mu}g)$ and liver cancer HEP-3B$(ED_{50};\;27{\mu}g)$.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.340.3-341
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• 2002

During the research for the development of antitumor agents. we found the 3-arylisoquinoline derivatives exhibited potent cytotoxicity against human tumor cell lines. For extending our study on these compounds. indeno［1.2-c］isoquinolines were chosen as the next research target due to previous studied data of the compounds that showed potent topoisomerase I inhibition activity as well as cytotoxicity against many kinds of tumor cell lines. Retrosynthetic consideration of indeno[1.2-d]isoquinolines indicates that the coupling of o-methyltoluamide with o-hydroxymethylbenxonitrile might afford 3-arylisoquinoline which could be translerred to the aldehtde. Indeno [1.2-c]isoquinolines can be formed by and inframolecular ring cyclization method. Various derlvatives of this compound including 11-alkoxy-6-methyl-6H. 11H-indeno[1.2-c]isoquinolin-5-one and biological activity will be presented with the docking model with topisomerase 1 enzyme.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.13 no.1
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• pp.129-140
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• 2000

ShingongNaetakSan(SNS) was drugs used in treatment of carbuncle and cellulitis in Oriental So, the purpose of this Study was to investigate effect of SNS on the proliferation of immunocytes and anti-cancer. This Study estimated the proliferation of L1210 cell lines and S-180 cell lines in vitro. and estimated the proliferation of L1210 cells, thymocytes and splenocytes, and tumor weight, body weight and mean survival rates in vivo. The proliferation and cytotoxicity of cells was tested using a colorimetric tetrazoliun assy(MTT assy). The results of this study were obtained as follow ; SNS had effect on the proliferation of L1210 cells in vitro and splenocytes in vivo, and SNS decreased significantly tumor weight, and increased significantly mean survival rates.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.2
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• pp.520-523
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• 2005

(R)-(-)-PGME amide of diterpene acid (2) was assigned the absolute configuration from NMR correlation experiments. The compound (2) was tested for its growth inhibitory effects against tumor cell lines by the MTT method.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.15 no.2
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• pp.132-144
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• 2002

Shinsuwuisaeng-Tang was a drug that treated carbuncle and cellulitis. So, the purpose of this Study was to investigate effect of Shinsuwuisaeng-Tang on the anti-cancer and nitric oxide(NO) production of peritoneal macrophages. We used Shinsuwuisaeng-Tang extract(SWT) with freeze-dried, 8wks-old male mice. and cancer cell lines(L1210, sarcoma-180) for this Study. The proliferation of cells was tested using a colorimetric tetrazoliun assay(MTT assay). The results of this Study were obtained as follow; SWT was showed cytotoxicity on the L1210 and sacoma-180(S-180) cell lines, SWT inhibited significantly proliferation of L1210 cells in L1210 cells transplanted mice, SWT accelerated NO production of peritoneal macrophages in L1210 cells transplanted mice. And SWT inhibited significantly tumor weight, increased significantly body weight and mean survival days in S-180 cells transplanted mice. This results suggest that SWT has anti-cancer by producing NO of peritoneal macrophages.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.2355-2362
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• 2012

The SH2B1 adaptor protein is recruited to multiple ligand-activated receptor tyrosine kinases that play important role in the physiologic and pathologic features of many cancers. The purpose of this study was to assess SH2B1 expression and to explore its contribution to the non-small cell lung cancer (NSCLC). Methods: SH2B1 expression in 114 primary NSCLC tissue specimens was analyzed by immunohistochemistry and correlated with clinicopathological parameters and patients' outcome. Additionally, 15 paired NSCLC background tissues, 5 NSCLC cell lines and a normal HBE cell line were evaluated for SH2B1 expression by RT-PCR and immunoblotting, immunofluorescence being applied for the cell lines. Results: SH2B1 was found to be overexpressed in NSCLC tissues and NSCLC cell lines. More importantly, high SH2B1 expression was significantly associated with tumor grade, tumor size, clinical stage, lymph node metastasis, and recurrence respectively. Survival analysis demonstrated that patients with high SH2B1 expression had both poorer disease-free survival and overall survival than other patients. Multivariate Cox regression analysis revealed that SH2B1 overexpression was an independent prognostic factor for patients with NSCLC. Conclusions: Our findings suggest that the SH2B1 protein may contribute to the malignant progression of NSCLC and could offer a novel prognostic indicator for patients with NSCLC.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3659-3665
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• 2014

To assess inhibition mechanisms of a Phellinus igniarius (PI) extract on cancer, C57BL/6 mice were orally treated with PI extractive after or before implanting H22 (hepatocellular carcinoma ) or B16 (melanoma) cells. Mice were orally gavaged with different doses of PI for 36 days 24h after introduction of H22 or B16 cells. Mice in another group were orally treated as above daily for 42 days and implanted with H22 cells on day 7. Then the T lymphocyte, antibody, cytokine, LAK, NK cell activity in spleen, tumor cell apoptosis status and tumor inhibition in related organs, as well as the expression of iNOS and PCNA in tumor tissue were examined. The PI extract could improve animal immunity as well as inhibit cancer cell growth and metastasis with a dose-response relationship. Notably, PI's regulation with the two kinds of tumor appeared to occur in different ways, since the antibody profile and tumor metastasis demonstrated variation between animals implanted with hepatocellular carcinoma and melanoma cells.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.4937-4944
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• 2015

MicroRNAs (miRNAs) are emerging as critical regulators in carcinogenesis and tumor progression. Recently, miR-99a has been reported as a tumor suppressor gene in various human cancers, but its functions in the context of anaplastic thyroid cancer (ATC) remain unknown. In this study, we reported that miR-99a was commonly downregulated in ATC tissue specimens and cell lines with important functional consequences. Overexpression of miR-99a not only dramatically reduced ATC cell viability by inducing cell apoptosis and accumulation of cells at G1 phase, but also inhibited tumorigenicity in vivo. We then screened and identified a novel miR-99a target, mammalian target of rapamycin (mTOR), and it was further confirmed by luciferase assay. Up-regulation of miR-99a would markedly reduce the expression of mTOR and its downstream phosphorylated proteins (p-4E-BP1 and p-S6K1). Similar to restoring miR-99a expression, mTOR down-regulation suppressed cell viability and increased cell apoptosis, whereas restoration of mTOR expression significantly reversed the miR-99a antitumor activity and the inhibition of mTOR/p-4E-BP1/p-S6K1 signal pathway profile. In clinical specimens and cell lines, mTOR was commonly overexpressed and its protein levels were statistically inversely correlated with miR-99a expression. Taken together, our results demonstrated for the first time that miR-99a functions as a tumor suppressor and plays an important role in inhibiting the tumorigenesis through targeting the mTOR/p-4E-BP1/p-S6K1 pathway in ATC cells. Given these, miR-99a may serve as a novel prognostic/diagnostic and therapeutic target for treating ATC.