• 제목/요약/키워드: Tumor suppression

검색결과 410건 처리시간 0.032초

Intratumoral Administration of Rhenium-188-Labeled Pullulan Acetate Nanoparticles (PAN) in Mice Bearing CT-26 Cancer Cells for Suppression of Tumor Growth

  • Song, Ho-Chun;Na, Kun;Park, Keun-Hong;Shin, Chan-Ho;Bom, Hee-Seung;Kang, Dong-Min;Kim, Sung-Won;Lee, Eun-Seong;Lee, Don-Haeng
    • Journal of Microbiology and Biotechnology
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    • 제16권10호
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    • pp.1491-1498
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    • 2006
  • The feasibility of pullulan acetate nanoparticles (PAN) with ionic strength (IS) sensitivity as a radioisotope carrier to inhibit tumor growth is demonstrated. PAN was radiolabeled with rhenium 188 (Re-188) without any chelating agents. The labeling efficiency of Re-188 into PAN (Re-188PAN) was $49.3{\pm}4.0%$ as determined by TLC. The tumor volumes of mice treated with 0.45 mCi of Re-188-PAN were measured and compared with that of free Re-188 after 5 days of intratumoral injection. For the histological evaluation of apoptotic nuclei of tumor cells, hematoxylin and eosin (H&E), and terminal deoxynucleotidyl transferase biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) staining were performed. The mean tumor volume of the Re-188-PAN-treated group was decreased by 36% after 5 days, whereas that the free Re-188-treated group was decreased by only 15% (P<0.05). The mean number of TUNEL-positive cells in Re-188-PAN-treated tumors at $144.3{\pm}79.9$ cells/section was significantly greater than the control ($26.7{\pm}7.9$ cells/section, P=0.03). The numbers of leukocyte and lymphocyte were decreased in both free Re-188- and Re-188-PAN-treated mice. These results indicated that the intratumoral injection of Re-188-PAN effectively inhibits the tumor growth by prolonging Re-188 retention time in tumor site induced by the IS sensitivity.

구강 편평상피암종에서 CDH-13 유전자의 promoter methylation에 대한 연구 (PROMOTER METHYLATION OF THE CDH-13 GENE IN THE ORAL SQUAMOUS CELL CARCINOMA)

  • 이문주;한세진;김경욱
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제34권5호
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    • pp.525-531
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    • 2008
  • CDH-13(T-cadherin), which is one of a kind among the 20 cadherins, can be found mainly in wall of aorta, neuron, spleen, blood vessel etc. It is also called H-cadherin. This structural difference can explain that CDH-13 is thought to play a key role in maintaining mutual relation between extra and intra-cellular environment rather than in cell adhesion. The main function of CDH-13 is to participate in blood vessel function. Additionally, it is known to regulate cell growth and cell contact inhibition. When cells are proliferating, cell surface perceives other cells so that substance such as CDH-13 can inhibit their growth or proliferation resulting in homeostasis without endless proliferation or invasion of connective tissue boundaries. However, tumor cell itself appears to be different from normal cells' growth, invasion or transmission. Therefore, it can be diagnosed that these characteristics are closely related to expression of CDH-13 in tumor cells. This study is to investigate expression of CDH-13 in SCC and its correlation with promoter methylation. 20 of tissue species for the study are excised and gathered from 20 patients who are diagnosed as SCC in department of OMS, dental hospital, dankook university. To find development of CDH-13 in each tissue samples, immunohistochemical staining, RT-PCR gene analysis and methylation specific PCR are processed. The results are as follows. 1.Immunohistochemical staining: In normal oral squamous epithelial tissue, strong expression of CDH-13 was found in cell plasma membrane of basal cell layer. On the other hand, in case of low-differentiated oral SCC, development of CDH-13 was hardly seen. 2.The development of CDH-13 gene: In 9 of samples, expression of CDH-13 gene could be seen and 2 of them showed low expression compared to the others. And rest of the 11 samples showed no expression of CDH-13 gene. 3.Methylation of CDH-13 gene: Among 9 samples which expressed CDH-13 gene, 7 of them showed unmethylation. In addition, among 11 samples without CDH-13 gene expression, 10 showed methylation. According to the results stated above, promoter methylation were found in 13 samples(65%) among 20 of oral SCC samples. In low-differentiated SCC, suppression of gene expression could be seen accompanying promoter methylation. These phenomenon of gene expression was proved by immunohistochemical investigation. Finally, for development of oral SCC, conclusions can be made that suppression of CDH-13 played a main role and suppression of gene expression was originated from promoter methylation. Considering this, it is expected that suppression of CDH-13 from promoter methylation to be utilized as a good diagnostic marker of oral SCC.

Palmitic acid inhibits inflammatory responses in lipopolysaccharide-stimulated mouse peritoneal macrophages

  • Lee, Ju-Young;Lee, Hye-Ja;Jeong, Ji-Ahn;Jung, Ji-Wook
    • Advances in Traditional Medicine
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    • 제10권1호
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    • pp.37-43
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    • 2010
  • Palmitic acid (PA) is one of free fatty acids, which is found from Gaultheria itoana Hayata and Sarcopyramis nepalensis. Although PA has a variety of pharmacological effects including mediates hypothalamic insulin resistance, induces IP-10 expression, and promote apoptotic activities, the anti-inflammatory mechanism of PA in mouse peritoneal macrophages remains unclear. In this study, we showed that PA exerted an anti-inflammatory action through suppression the production of tumor necrosis factor-$\alpha$, interleukin-6, cyclooxygenases-2 and nitric oxide in lipopolysaccaride-stimulated mouse peritoneal macrophages. Our study suggests an important molecular mechanism of PA, which might explain its beneficial effect in the regulation of inflammatory reactions.

Inhibitory Effect of Esculetin on the Inducuble Nitric Oxide Synthase Expression in TNF-stimulated 3T3-L1 Adipocytes

  • Yang, Jeong-Yeh
    • The Korean Journal of Physiology and Pharmacology
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    • 제7권5호
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    • pp.283-287
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    • 2003
  • While nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) is beneficial for host survival, it is also detrimental to the host. Thus, regulation of iNOS gene expression may be an effective therapeutic strategy for the prevention of unwanted reactions at various pathologic conditions. During the screening process for the possible iNOS regulators, we observed that esculetin is a potent inhibitor of cytokine-induced iNOS expression. The treatment of 3T3-L1 adipocytes with the tumor necrosis factor-${\alpha}$ (TNF) induced iNOS expression, leading to enhanced NO production. TNF-induced NO production was inhibited by esculetin in a dose-dependent manner. Esculetin inhibited the TNF-induced NO production at the transcriptional level through suppression of iNOS mRNA and subsequent iNOS protein expression. These results suggest esculetin, a component of natural products, as a naturally occurring, nontoxic means to attenuate iNOS expression and NO-mediated cytotoxicity.

Antitumor Effects of Glycoportein Extracted from Sea Cucumber (Stichopus japonicus)

  • Moon, Jeung-Hye;Ryu, Hong-Sool;Suh, Jae-Soo
    • Preventive Nutrition and Food Science
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    • 제4권2호
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    • pp.117-121
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    • 1999
  • The anititumor and immunologic activities of the glycoproteins extracted from sea cucumber (Stichopus japonicus) on mice bearing sarcoma 180 cells were investigated . Maximum tumor suppression (64%) occurred at the dose of 100mg glycoprotein/kg. The highest prolongation ratio was achieved at the level of 100mg/kg an dincreased by 395 more than that of control. Glycoproteins from sea cucumber exhibited direct cytotoxic effect on the tumor cells. Dose dependent increase of leucocyte, peritoneal exudate cell and weights of immunoorgans revealed the improvement of immunity. When the glycoportein-administered group was compared with the control, a significant difference was not noted in the clinico-chemical values such as S-GOT, S-GPT , alkaline phoshatse activity, total protein, cholesterol, triglyceride, urea nitrogen and glucose levels in blood. These results suggests that the antitumor activity of sea cucumber glycoprotein is associated with activation of cells in the immune system.

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Intramedullary Spinal Cord Lipoma Extending from the Cervicomedullary Junction to the Upper Thoracic Cord

  • Lee, Deok-Gu;Yoon, Seok-Mann;Shim, Jai-Joon;Bae, Hack-Gun
    • Journal of Korean Neurosurgical Society
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    • 제38권1호
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    • pp.71-73
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    • 2005
  • A case of intramedullary spinal cord lipoma is presented. A one month-old male infant presented with irritability and weakness on his upper extremities. A magnetic resonance[MR] image of the cervical spine demonstrated a well defined, high signal intensity lesion on both T1 and T2-weighted MR images and suppression on the fat saturation sequence. The tumor mass extended from the foramen magnum to T2 vertebra level. Ventral displacement of the spinal cord with kinking of the cervico-medullary junction was evident on the T2-weighted sagittal image. Partial resection of the tumor mass through laminoplastic laminotomy from C1 to T2 resulted in improved motor weakness on his upper extremities.

Immune Evasion of G-CSF and GM-CSF in Lung Cancer

  • Yeonhee Park;Chaeuk Chung
    • Tuberculosis and Respiratory Diseases
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    • 제87권1호
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    • pp.22-30
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    • 2024
  • Tumor immune evasion is a complex process that involves various mechanisms, such as antigen recognition restriction, immune system suppression, and T cell exhaustion. The tumor microenvironment contains various immune cells involved in immune evasion. Recent studies have demonstrated that granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) induce immune evasion in lung cancer by modulating neutrophils and myeloid-derived suppressor cells. Here we describe the origin and function of G-CSF and GM-CSF, particularly their role in immune evasion in lung cancer. In addition, their effects on programmed death-ligand 1 expression and clinical implications are discussed.

암세포 표적지향화를 위한 항체-엔도스타틴 융합단백질의 체내동태 및 종양으로의 이행성 (In Vivo Tumor Cell Distribution of Antibody-Endostatin Fusion Protein for Tumor-Specific Targeting and Pharmacokinetics)

  • 강영숙;이나영
    • Journal of Pharmaceutical Investigation
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    • 제33권4호
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    • pp.287-292
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    • 2003
  • A novel antitumor agent, antibody-endostatin fusion protein $(anti-HER2/neu\;IgG3C_H3-Endostatin,\;AEFP)$ formed by genetic engineering procedure from antibody (Ab) which specifically targets to tumor cells ad angiogenesis inhibitor, endostatin (Endo) that has excellent antitumor effect, minimizes the toxicity of normal cells and selectively kills only tumor cells. The purpose of this study is to evaluate the phamacokinetic parameters and to analyze the localization of AEFP. After an intravenous injection of $150\;{\mu}l\;(5\;{\mu}Ci)\;[^{125}I]Ab,\;[^{125}I]AEFP$ to mice, blood was collected though retroorbital plexus from 15 min to 2880 min. Following the jugular vein injetion of $150\;{\mu}l\;(10\;{\mu}Ci)\;[^{125}I]Endo$, blood was collected by the use of carotid artery cannulation from 0.25 min to 30 min. Consequently, Endo was very rapidly removed from plasma compartment within 30 min. On the other hand, AEFP similar to Ab was slowly cleared from plasma. Also, Endo was metabolized about 40% within 30 min. However, AEFP was shown to metabolize less than 10% within 2880 min. The organ distribution of Endo was in order kidney, lung, spleen. Both Ab and AEFP were localized in order spleen, kidney, liver. Futhermore the tumor/blood distribution ratio of AEFP at 96 hours after injection is about 20 times higher than it of Endo at one hour after injection. In conclusion, these studies demonstrate that the anti-cancer or suppression of angiogenesis effect of Endo may be improved by the use of AEFP because the longer half life and stability of AEFP is able to selectively target antigens expressed on tumors.

전이성 혈관주위세포종 환자에서 발생한 저혈당을 프레드니솔론으로 치료한 1예 (Treatment of Hemangiopericytoma-Associated Hypoglycemia with Glucocorticoid Therapy)

  • 박성우;김동근;김명진;장효진;손세훈;고성애;이하영;김민경;이경희;현명수
    • Journal of Yeungnam Medical Science
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    • 제28권1호
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    • pp.77-83
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    • 2011
  • Non-islet cell tumor-induced hypoglycemia (NICTH) is associated with mesenchymal tumor types, including hemangiopericytoma, fibrosarcoma, mesothelioma, and neurofibroma, as well as carcinoma of the liver, adrenal glands, and kidneys. Non- islet cell tumors induce hypoglycemia by overproducing an abnormal form of insulin-like growth factor II (IGF m. Complete removal of the tumor or reduction of the tumor mass is a successful therapeutic strategy in cases of NICTH. However, if the tumor re-grows, curative resection is nearly impossible, and hypoglycemia occurs repeatedly. Glucocorticoids are effective in terms of long-term relief from hypoglycemia through promotion of gluconeogenesis in the liver, tumor suppression, production of 'big'-IGF-II, and correction of the attendant biochemical abnormalities involving the growth hormone (GH)-IGF axis. We found that administration of corticosteroid therapy to a patient suffering from NICTH resulted in improvement of hypoglycemia associated symptoms.

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NDRG2 Expression Decreases Tumor-Induced Osteoclast Differentiation by Down-regulating ICAM1 in Breast Cancer Cells

  • Kim, Bomi;Nam, Sorim;Lim, Ji Hyun;Lim, Jong-Seok
    • Biomolecules & Therapeutics
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    • 제24권1호
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    • pp.9-18
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    • 2016
  • Bone matrix is properly maintained by osteoclasts and osteoblasts. In the tumor microenvironment, osteoclasts are increasingly differentiated by the various ligands and cytokines secreted from the metastasized cancer cells at the bone metastasis niche. The activated osteoclasts generate osteolytic lesions. For this reason, studies focusing on the differentiation of osteoclasts are important to reduce bone destruction by tumor metastasis. The N-myc downstream-regulated gene 2 (NDRG2) has been known to contribute to the suppression of tumor growth and metastasis, but the precise role of NDRG2 in osteoclast differentiation induced by cancer cells has not been elucidated. In this study, we demonstrate that NDRG2 expression in breast cancer cells has an inhibitory effect on osteoclast differentiation. RAW 264.7 cells, which are monocytic preosteoclast cells, treated with the conditioned media (CM) of murine breast cancer cells (4T1) expressing NDRG2 are less differentiated into the multinucleated osteoclast-like cells than those treated with the CM of 4T1-WT or 4T1-mock cells. Interestingly, 4T1 cells stably expressing NDRG2 showed a decreased mRNA and protein level of intercellular adhesion molecule 1 (ICAM1), which is known to enhance osteoclast maturation. Osteoclast differentiation was also reduced by ICAM1 knockdown in 4T1 cells. In addition, blocking the interaction between soluble ICAM1 and ICAM1 receptors significantly decreased osteoclastogenesis of RAW 264.7 cells in the tumor environment. Collectively, these results suggest that the reduction of ICAM1 expression by NDRG2 in breast cancer cells decreases osteoclast differentiation, and demonstrate that excessive bone resorption could be inhibited via ICAM1 down-regulation by NDRG2 expression.