• Title/Summary/Keyword: Cell treatment

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Exosomes Secreted by Toxoplasma gondii-Infected L6 Cells: Their Effects on Host Cell Proliferation and Cell Cycle Changes

  • Kim, Min Jae;Jung, Bong-Kwang;Cho, Jaeeun;Song, Hyemi;Pyo, Kyung-Ho;Lee, Ji Min;Kim, Min-Kyung;Chai, Jong-Yil
    • Parasites, Hosts and Diseases
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    • v.54 no.2
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    • pp.147-154
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    • 2016
  • Toxoplasma gondii infection induces alteration of the host cell cycle and cell proliferation. These changes are not only seen in directly invaded host cells but also in neighboring cells. We tried to identify whether this alteration can be mediated by exosomes secreted by T. gondii-infected host cells. L6 cells, a rat myoblast cell line, and RH strain of T. gondii were selected for this study. L6 cells were infected with or without T. gondii to isolate exosomes. The cellular growth patterns were identified by cell counting with trypan blue under confocal microscopy, and cell cycle changes were investigated by flow cytometry. L6 cells infected with T. gondii showed decreased proliferation compared to uninfected L6 cells and revealed a tendency to stay at S or G2/M cell phase. The treatment of exosomes isolated from T. gondii-infected cells showed attenuation of cell proliferation and slight enhancement of S phase in L6 cells. The cell cycle alteration was not as obvious as reduction of the cell proliferation by the exosome treatment. These changes were transient and disappeared at 48 hr after the exosome treatment. Microarray analysis and web-based tools indicated that various exosomal miRNAs were crucial for the regulation of target genes related to cell proliferation. Collectively, our study demonstrated that the exosomes originating from T. gondii could change the host cell proliferation and alter the host cell cycle.

ANTI-TUMOR EFFECTS OF VASCULAR ENDOTHELIAL GROWTH FACTOR INHIBITOR ON ORAL SQUAMOUS CELL CARCINOMA CELL LINES (혈관내피세포성장인자 억제제에 의한 구강편평상피세포암종 세포주의 성장 억제 효과)

  • Han, Se-Jin;Lee, Jae-Hoon
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.35 no.2
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    • pp.66-73
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    • 2009
  • Tumor angiogenesis is a process leading to formation of blood vessels within tumors and is crucial for maintaining a supply of oxygen and nutrients to support tumor growth and metastasis. Vascular endothelial growth factor(VEGF) plays a key role in tumor angiogenesis including induction of endothelial cell proliferation, migration, survival and capillary tube formation. VEGF binds to two distinct receptors on endothelial cells. VEGFR-2 is considered to be the dominant signaling receptor for endothelial cell permeability, proliferation, and differentiation. Bevacizumab(Avastin, Genetech, USA) is a monoclonal antibody against vascular endothelial growth factor. It is used in the treatment of cancer, where it inhibits tumor growth by blocking the formation of new blood vessels. The goal of this study is to identify the anti-tumor effect of Bevacizumab(Avastin) for oral squamous cell carcinoma cell lines. Human squamous cell carcinoma cell line(HN4) was used in this study. We examined the sensitivity of HN4 cell line to Bevacizumab(Avastin) by using in vitro proliferation assays. The results were as follows. 1. In the result of MTT assay according to concentration of Bevacizumab(Avastin), antiproliferative effect for oral squamous cell carcinoma cell lines was observed. 2. The growth curve of cell line showed the gradual growth inhibition of oral squamous cell carcinoma cell lines after exposure of Bevacizumab(Avastin). 3. In the apoptotic index, groups inoculated Bevacizumab(Avastin) were higher than control groups. 4. In condition of serum starvation, VEGFR-2 did not show any detectable autophosphorylation, whereas the addition of VEGF activated the receptor. Suppression of phosphorylated VEGFR-2 and phosphorylated MAPK was observed following treatment with Bevacizumab(Avastin) in a dose-dependent manner. 5. In TEM view, dispersed nuclear membrane, scattered many cytoplasmic vacuoles and localized chromosomal margination after Bevacizumab(Avastin) treatment were observed. These findings suggest that Bevacizumab(Avastin) has the potential to inhibit MAPK pathway in proliferation of oral squamous cell carcinoma cell lines via inhibition of VEGF-dependent tumor growth.

Surgical treatment of Giant Cell Tumor in Knee Joint (슬관절 주위 거대세포종의 치료)

  • Bae, Dae-Kyung
    • The Journal of the Korean bone and joint tumor society
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    • v.1 no.1
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    • pp.1-6
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    • 1995
  • Giant cell tumors are primary bone tumors originating from non-osteoblastic connective tissue. The sites of involvement were commonly distal femur, proximal tibia, proximal humerus, distal radius and others (including os calcis, ilium and sacrum). Giant cell tumor located around knee joint has been difficult to treat because of local recurrence following curettage with or without bone graft. Although primary resections reduce recurrence of the lesion, the joint function will be markedly impaired. Marginal excision was very often complicated by a loss of joint integrity since all the giant cell tumors occupy juxtaarticular positions. Techniques involving physical adjuncts(high speed burr and electric cauterization) have been used in the hope of decreasing the rate of local recurrence and avoiding the morbidity of primary resection. A meticulous clinical, radiological and histological evaluation is needed to choose the correct treatment, keeping in mind the possibility of recurrence after each treatment modality.

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Advanced Lake Water Treatment with Bipolar Packed Bed Electrode Cell(II) (3차원 전극(Bipolar Packed Bed Electrode)을 이용한 호소수 처리(II))

  • 장철현;박상우;최창수
    • Journal of Environmental Science International
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    • v.11 no.4
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    • pp.355-360
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    • 2002
  • This study was to analyze the right of wrong of gray-water treatment by applying BPBE electrode cell to the effluence water in the terminal disposal plant of sewage. The results were as follows : The best result was obtained with applied voltage 40V and detention time 6 minutes for the BPBE electrode cell which has the graphite-plate in main electro-de, packing coconut activated carbon. The elimination rate of COD of Al-plate was higher than that of graphite-plate in main electrode. The result of electrolysis for 3 hour in parallel circuit showed the using possibility of gray-water according to each elimination rate : COD 59%, T-N 69 %, T-P 69%. The BPBE electrode cell with the Al-plate in main electrode made the best effect for the elimination of algae in lake water and algae were not occurred in electrolytic water.

The Study on Acute and Subacute Toxicity and Sarcoma-180 Anti-cancer Effects of Carthami Tinctor-Fructus Herbal-acupuncture(CF) (홍화자약침(紅花子藥鍼)의 급성(急性) 아급성(亞急性) 독성실험(毒性實驗) 및 Sarcoma-180 항암효과(抗癌效果)에 관(關)한 실험적(實驗的) 연구(硏究))

  • An, Chang-Suk;Kwon, Ki-Rok;Lee, Seon-Goo
    • Journal of Pharmacopuncture
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    • v.5 no.1 s.8
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    • pp.7-26
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    • 2002
  • Objective: The purpose of this study was to investigate acute and subacute toxicity and sarcoma-180 anti-cancer effects of herbal acupuncture with Carthami- Tinctorii fructus (CF) in mice and rats. Method: Balb/c mice were injected intraperitoneally with Carthami - Tinctorii fructus (CF) for $LD_{50}$ and acute toxicity test. Sprague Dawley rats were injected intraperitoneally with Carthami- Tinctorii fructus (CF) for subacute toxicity test. The Carthami- Tinctorii fructus herbal-acupuncture was injected on Chung-wan (CV12) of mice with Sarcoma-180 cancer cell line. Results: 1. $LD_{50}$ was uncountable as none of the subjects expired during the test. 2. In acute toxicity test, toxic symptoms were not detected, but the body weight of mice was increased in treatment Ⅰ, treatment Ⅱ groups, compared to the normal group.(p<0.05) 3. In acute toxicity test of serum biochemical values of mice, glucose was increased in treatment Ⅰ and treatment Ⅱ groups, total cholesterol was increased in treatment I group, GOT was decreased in treatment Ⅱ group, and GPT was decreased in treatment Ⅰ group, compared to the normal group.(p<0.05) 4. The clinical signs and the body weight of mice treated with 0.1 cc, 0.2cc Carthami- Tinctorii fructus (CF) were not affected during the subacute toxicity test. 5. In subacute toxicity test, treatment groups didn't show significant changes in complete blood count test (CBC) of rats, compared to the nonnal group.(p<0.05) 6. In subacute toxicity test of serum biochemical values of rats, uric acid was decreased in treatment Ⅰ and treatment Ⅱ groups, compared to the nonnal group, triglyceride was decreased in treatment I group, compared to the normal group, GOT and GPT were decreased in treatment I and treatment Ⅱ groups, and alkaline phosphatase was decreased in treatment Ⅰ and treatment Ⅱ groups, compared to the normal group.(p<0.05) 7. Median survival time was increased in all the treatment groups for Sarcoma-180 cancer cell treated with Carthmni- Tinctorii fructus (CF).(p<0.05) 8. Natural killer cell activity was significantly increased in all the treatment groups compared to the normal group.(p<0.05) 9. Interleukin-2 productivity was decreased in treatment Ⅰ and treatment Ⅱ groups.(p<0.05) Conclusion: According to the results, we can conclude herbal-acupuncture of Carthami-Tinctoriifructus (CF) caused negligible toxkity, and had anti-tumor effects in mice.

Cell Cycle and Cancer

  • Park, Moon-Taek;Lee, Su-Jae
    • BMB Reports
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    • v.36 no.1
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    • pp.60-65
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    • 2003
  • Cancer is frequently considered to be a disease of the cell cycle. As such, it is not surprising that the deregulation of the cell cycle is one of the most frequent alterations during tumor development. Cell cycle progression is a highly-ordered and tightly-regulated process that involves multiple checkpoints that assess extracellular growth signals, cell size, and DNA integrity. Cyclin-dependent kinases (CDKs) and their cyclin partners are positive regulators of accelerators that induce cell cycle progression; whereas, cyclin-dependent kinase inhibitors (CKIs) that act as brakes to stop cell cycle progression in response to regulatory signals are important negative regulators. Cancer originates from the abnormal expression of activation of positive regulators and functional suppression of negative regulators. Therefore, understanding the molecular mechanisms of the deregulation of cell cycle progression in cancer can provide important insights into how normal cells become tumorigenic, as well as how cancer treatment strategies can be designed.

Acupuncture Suppresses Intrastriatal Hemorrhage-Induced Neuronal Cell Death and Proliferation in Rats

  • Cho, Nam-Hun;Park, Dong-suk;Lee, Jae-Dong
    • The Journal of Korean Medicine
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    • v.24 no.4
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    • pp.127-135
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    • 2003
  • Objectives : Intracerebral hemorrhage (ICH) is one of the most devastating types of stroke. The effect of acupuncture on the intrastriatal hemorrhage-induced neuronal cell death and cell proliferation in rats is examined. Methods : Cell death and cell proliferation in rats was investigated via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and immunohistochemistry for caspase-3 and 5-bromo-2'-deoxyuridine (BrdU). Results : Results showed that apoptotic cell death in the striatum and cell proliferation in the hippocampal dentate gyrus significantly increased following intrastriatal hemorrhage in rats, and that acupunctural treatment at the Zusanli acupoint suppressed the hemorrhage-induced increase in apoptosis in the striatum and cell proliferation in the dentate gyrus. Conclusions : It is suggested that acupunctural treatment, especially at the Zusanli acupoint, may aid recovery following central nervous system sequelae following ICH.

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Induction of Cdk inhibitor p27 and Inhibition of pRB Phosphorylation by Insamsapye-tang Treatment in Human Lung Cancer A549 Cells (인체 폐암세포에서 인삼사폐탕에 의한 Cdk inhibitor p27의 발현 증가 및 pRB의 인산화 억제)

  • Lee Min Woo;Seo Chang Hun;Park Cheol;Lee Won Ho;Choi Yung Hyun;Park Dong Il
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.1
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    • pp.213-219
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    • 2003
  • We investigated the effects of Insamsapye-tang (ISSPT) water extract on the cell proliferation of human lung carcinoma A549 cells. ISSPT treatment resulted in the inhibition of cell proliferation in a concentration-dependent manner. This anti-proliferative effect of A549 cells by ISSSPT treatment was associated with morphological changes such as membrane shrinking and cell rounding up. DNA flow cytometric histograms showed that population of G1 phase of the cell cycle was increased by ISSPT treatment in a concentration-dependent manner. ISSPT treatment induced the levels of tumor suppressor p53 protein and cyclin-dependent kinase (Cdk) inhibitor p27 without significant alteration of cyclins and Cdks expression. In addition, ISSPT treatment resulted in down-regulation of phosphorylated retinoblastoma protein (pRB). However, the levels of p130, the pRB family protein, and transcription factors. E2F-1 and E2F-4. were remained unchanged. The present results indicated that ISSPT-induced inhibition of lung cancer cell proliferation is associated with the blockage of G1/S progression and the induction of apoptosis, and we suggest that ISSPT will be an effective therapeutic agent on human lung cancer.

Endoplasmic Reticulum (ER) Stress Inhibitor or Antioxidant Treatments during Micromanipulation Can Inhibit Both ER and Oxidative Stresses in Porcine SCNT Embryos

  • Park, Hye-Bin;Park, Yeo-Reum;Kim, Mi-Jeong;Jung, Bae-Dong;Park, Choon-Keun;Cheong, Hee-Tae
    • Development and Reproduction
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    • v.24 no.1
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    • pp.31-41
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    • 2020
  • We investigated the effects of endoplasmic reticulum (ER) stress inhibitor and antioxidant treatments during the micromanipulation of somatic cell nuclear transfer (SCNT) on in vitro development of SCNT embryos. Tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor and vitamin C (Vit. C), an antioxidant, were treated by alone or in combination, then, the level of X-box binding protein 1 (Xbp1) splicing and the expressions of ER stress-associated genes, oxidative stress-related genes, and apoptotic genes were confirmed in the 1-cell and blastocyst stages. In the 1-cell stage, the levels of Xbp1 splicing were significantly decreased in TUDCA and Vit. C treatment groups compared to the control (p<0.05). In addition, the expression levels of most ER stress-associated genes and oxidative stress-related genes were significantly lower in all treatment groups than the control (p<0.05), and the transcript levels of apoptotic genes were also significantly lower in all treatment groups than the control (p<0.05). In the blastocyst stage, decreased expression of ER stress-, oxidative stress-, and apoptosis-related genes were observed only in some treatments. However, the blastocyst formation rates in TUDCA and Vit. C treatment groups (24.8% and 22.0%, respectively) and mean blastocyst cell number in all treatment groups (59.7±4.3 to 63.5±3.3) were significantly higher (p<0.05) than those of control. The results showed that the TUDCA or Vit. C treatment during micromanipulation inhibited both ER and oxidative stresses in the early stage of SCNT embryos, thereby reducing cell damage and promoting in vitro development.

Glucocorticoid treatment independently affects expansion and transdifferentiation of porcine neonatal pancreas cell clusters

  • Kim, Ji-Won;Sun, Cheng-Lin;Jeon, Sung-Yoon;You, Young-Hye;Shin, Ju-Young;Lee, Seung-Hwan;Cho, Jae-Hyoung;Park, Chung-Gyu;Yoon, Kun-Ho
    • BMB Reports
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    • v.45 no.1
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    • pp.51-56
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    • 2012
  • The purpose of this study was to determine the effects of duration and timing of glucocorticoid treatment on the expansion and differentiation of porcine neonatal pancreas cell clusters (NPCCs) into ${\beta}$-cells. After transplantation of NPCCs, the ductal cyst area and ${\beta}$-cell mass in the grafts both showed positive and negative correlations with duration of dexamethasone (Dx) treatment. Pdx-1 and HNF-3${\beta}$ gene expression was significantly downregulated following Dx treatment, whereas PGC-1${\alpha}$ expression increased. Pancreatic duct cell apoptosis significantly increased following Dx treatment, whereas proliferation did not change. Altogether, transdifferentiation of porcine NPCCs into ${\beta}$-cells was influenced by the duration of Dx treatment, which might have been due to the suppression of key pancreatic transcription factors. PGC-1${\alpha}$ plays an important role in the expansion and transdifferentiation of porcine NPCCs, and the initial 2 weeks following transplantation of porcine NPCCs is a critical period in determining the final ${\beta}$-cell mass in grafts.