• Title/Summary/Keyword: cell-cycle inhibition

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Current Status of Bacterial Brown Stripe of Rice Caused by Acidovorax avenae subsp. avenae (Acidovorax avenae subsp. avenae에 의한 세균성줄무늬병의 연구동향)

  • 송완엽
    • Plant Disease and Agriculture
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    • v.5 no.2
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    • pp.69-76
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    • 1999
  • Acidovorax avenae subsp. avenae is the causal pathogen of several hosts including oats corn foxtail millet wheatgrass sugarcane and rice. The pathogen is a seedborne pathogen of rice and known to occur widely in rice growing countries. The pathogen cause inhibition of germination brown stripe on the leaf curling of the leaf sheath and abnormal elongation of the mesocotyl of irce. Bacterial colonies grow slowly and are convex circular and creamy with tan to brown center. The causal baterium is Gram-negative and rod shape with a single polar flagellum Nonfluorescence poly-$\beta$-hydroxybutyrate accumulation and precipitate formation around the colony on the medium are useful in the differentiation of this bacterium from other subspecies of A. avenae as well as nonfluorescent bacteria pathogenic to rice. This bacterium has belonged to the genus of Psdeudomonas but recently was transferred to the new genus Acidovorax on the basis of bacteriological and molecular biological data. However the difference of biochemical characteristics protein profile of the cell and host range among strains should be more clarified. To develop an effective control strategy for this disease understanding of detailed life cycle of the disease ritical environmental factors affecting disease development on each host and relationship to grain discoloration of rice are prerequisite. Although the affected area has been world-widely reported there is on recent progress on the understanding of the bacteriological and ecological characteristics of the causal bacterium and control means of the disease.

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?Effects of Duchesnea indica on Several Kinds of Cancer Cells (사매가 수종(數種)의 암세포(癌細胞)에 미치는 영향(影響))

  • Kim, Yun-Kwan;Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Ki-Won;Ryu, Bong-Ha
    • The Journal of Internal Korean Medicine
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    • v.26 no.2
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    • pp.320-332
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    • 2005
  • Objectives: The aim of the experiment is to identify any anti-tumor effects of Duchesnea indica(Andr.) Focke on stomach, liver, urinary bladder, prostate and kidney cancer cells. Materials & Methods: For cancer cells, AGS stomach, Hep3B and Hep3G2 liver, HT-1197, HT-1376 urinary bladder, PC3 prostate, and A-704 kidney cancer cells, all obtained from Korean Ce 11 Line Bank, were used. The boiled extract of Duchesnea indica(Andr.) Focke (10 and 20 microliters) was injected into cultures, and the cultures were observed at 0, 6 and 12 hours, and from then on at 12 hours intervals up to 72 hours. The destruction of stomach, liver, urinary bladder, prostate and kidney cancer cells were measured through Trypan blue exclusion testing. The suppresion on viability of stomach, liver, urinary bladder, prostate and kidney cancer cells was measured via MTT assay. Anti-cancer mechanisms were assessed by analyzing the cell cycle. Results: In morphologic change, AGS, Hep3B, HepG2 showed the withdrawn and floating appearance that is typical in cellular impairment. The destruction of AGS, HT-1197, HT-1376, A-704, PC-3, Hep3B and HepG2 cancer cells in each test group was greater than that in the control group to a statistically significant degree. The suppression on viability of AGS, HT-1197 and Hep3G in each test group was greater than that in the control group to a statistically significant degree. Analysis of the cell cycle after injection of D... Focke showed inhibition of cell division in all test groups(AGS, Hep3B, HepG2, HT-1197, HT-1376, PC3, A-704). Conclusions: The results of this experiment suggest that Duchesnea indica(Andr.) Focke has statistically significant anti-tumor effects on stomach, urinary bladder, kidney, prostate and liver cancer, of which stomach and liver cancer are prominently significant. This in vitro experiment supports a role for Duchesnea indica(Andr.) Focke as a potential cancer treatment, but progressive research on Duchesnea indica(Andr.) Focke and its anti-tumor effects is needed to develop a practical application for it in cancer treatment.

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Anti-proliferative Effects of the Isothiocyanate Sulforaphane on the Growth of Human Cervical Carcinoma HeLa Cells (Sulforaphane에 의한 HeLa 인체자궁경부함세포의 증식 억제 기전 연구)

  • Park Soung Young;Bae Song-Ja;Choi Yung Hyun
    • Journal of Life Science
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    • v.15 no.3 s.70
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    • pp.397-405
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    • 2005
  • Sulforaphane, an isothiocyanate derived from hydrolysis of glucoraphanin in broccoli and other cruciferous vegetables, was shown to induce phase II detoxification enzymes and inhibit chemically induced mammary tumors in rodents. Recently, sulforaphane is known to induce cell cycle arrest and apoptosis in human cancer cells, however its molecular mechanisms are poorly understood. In the present study, we demonstrated that sulforaphane acted to inhibit proliferation and induce morphological changes of human cervical carcinoma HeLa cells. Treatment of HeLa cells with $10{\mu}M\;or\;15{\mu}M$ sulforaphane resulted in significant G2/M cell cycle arrest as determined by flow cytometry. Moreover, $20{\mu}M$ sulforaphane significantly induced the population of sub-G1 cells (9.83 fold of control). This anti-proliferative effect of sulforaphane was accompanied by a marked inhibition of cyclin A and cyclin-dependent kinase (Cdk)4 protein and concomitant induction of Cdc2, Cdk inhibitor p16 and p21. However, sulforaphane did not affect the levels of cyelooxygenases and telomere-regulatory gene products. Although further studies are needed, the present work suggests that sulforaphane may be a potential chemoprevetive/ chemotherapeutic agent for the treatment of human cancer cells.

Constitutive Activation of $p70^{S6k}$ in Cancer Cells

  • Kwon, Hyoung-Keun;Bae, Gyu-Un;Yoon, Jong-Woo;Kim, Yong-Kee;Lee, Hoi-Young;Lee, Hyang-Woo;Han, Jeung-Whan
    • Archives of Pharmacal Research
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    • v.25 no.5
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    • pp.685-690
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    • 2002
  • The mitogen-stimulated serine/threonine kinase $p70^{S6k}$ plays an important role in the progression of cells from $G_0/G$_1$$ to S phase of the cell cycle by translational up-regulation of a family of mRNA transcripts family of mRNA transcripts which contain polypyrimidine tract at their 5 transcriptional start site. Here, we report that $p70^{S6k}$ was constitutively phosphorylated and activated to various degrees in serum-deprived AGS, A2058, HT-1376, MG63, MCF7, MDA-MB-435S, MDA-MB-231 and MB-157. Rapamycin treatment induced a significant dephosphorylation and inactivation of $p70^{S6k}$ in all cancer cell lines, while wortmannin, a specific inhibitor of PI3-K, caused a mild dephosphorylation of $p70^{S6k}$ in AGS, MDA-MB-435S and MB-157. In addition, SQ20006, methylxanthine phosphodiesterase inhibitor, reduced the phosphorylation of $p70^{S6k}$ in all cancer cells tested. Consistent with inhibitory effect of rapamycin on $p70^{S6k}$ activity, rapamycin inhibited [$^3H$]-thymidine incorporation and increased the number of cells at $G_{0}G_{1}$ phase. Furthermore, these inhibitory effects were accompanied by the decrease in growth of cancer cells. Taken together, the results indicate that the antiproliferative activity of rapamycin might be attributed to cell cycle arrest at $G_{0}G_{1}$ phase in human cancer cells through the inhibition of constitutively activated $p70^{S6k}$ of cancer cells and suggest $p70^{S6k}$ as a potential target for therapeutic strategies aimed at preventing or inhibiting tumor growth.

Fisetin Protects C2C12 Mouse Myoblasts from Oxidative Stress-Induced Cytotoxicity through Regulation of the Nrf2/HO-1 Signaling

  • Cheol Park;Hee-Jae Cha;Da Hye Kim;Chan-Young Kwon;Shin-Hyung Park;Su Hyun Hong;EunJin Bang;Jaehun Cheong;Gi-Young Kim;Yung Hyun Choi
    • Journal of Microbiology and Biotechnology
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    • v.33 no.5
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    • pp.591-599
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    • 2023
  • Fisetin is a bioactive flavonol molecule and has been shown to have antioxidant potential, but its efficacy has not been fully validated. The aim of the present study was to investigate the protective efficacy of fisetin on C2C12 murine myoblastjdusts under hydrogen peroxide (H2O2)-induced oxidative damage. The results revealed that fisetin significantly weakened H2O2-induced cell viability inhibition and DNA damage while blocking reactive oxygen species (ROS) generation. Fisetin also significantly alleviated cell cycle arrest by H2O2 treatment through by reversing the upregulation of p21WAF1/CIP1 expression and the downregulation of cyclin A and B levels. In addition, fisetin significantly blocked apoptosis induced by H2O2 through increasing the Bcl-2/Bax ratio and attenuating mitochondrial damage, which was accompanied by inactivation of caspase-3 and suppression of poly(ADP-ribose) polymerase cleavage. Furthermore, fisetin-induced nuclear translocation and phosphorylation of Nrf2 were related to the increased expression and activation of heme oxygenase-1 (HO-1) in H2O2-stimulated C2C12 myoblasts. However, the protective efficacy of fisetin on H2O2-mediated cytotoxicity, including cell cycle arrest, apoptosis and mitochondrial dysfunction, were greatly offset when HO-1 activity was artificially inhibited. Therefore, our results indicate that fisetin as an Nrf2 activator effectively abrogated oxidative stress-mediated damage in C2C12 myoblasts.

Inhibitory Effects of Illicium verum Hooker fil. Dichloromethane Fractions on Adipocyte Differentiation (팔각회향 dichloromethane 분획물에 의한 지방세포 분화 억제 효과)

  • Jeong, Hyun Young;Jeong, In Kyo;Kim, Nam Ju;Yun, Hee Jung;Park, Jung Ha;Kim, Byung Woo;Kwon, Hyun Ju
    • Journal of Life Science
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    • v.29 no.4
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    • pp.447-454
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    • 2019
  • Fat accumulation in adipocytes occurs through the process of adipogenesis in which preadipocytes differentiate into adipocytes. Obesity is a metabolic disorder caused by excessive accumulation of fat in the body, which increases the incidence of cardiovascular diseases, hypertension, type 2 diabetes, hyperlipidemia, and various cancers. Recently, inhibition of adipocyte differentiation was shown to be a potential antiobesity strategy. In this study, the inhibitory effect of dichloromethane fractions from Illicium verum Hooker fil. water extract on the differentiation of 3T3-L1 preadipocytes to adipocytes was investigated. Dichloromethane fractions from I. verum Hooker fil. significantly inhibited adipocyte differentiation when applied during the adipocyte differentiation process, as assessed by measuring fat accumulation using Oil-red O staining. In addition, dichloromethane fractions from I. verum Hooker fil. reduced important adipogenic transcription factors, such as CCAAT/enhancer binding protein ${\alpha}$ ($C/EBP{\alpha}$), $C/EBP{\beta}$, and peroxisome proliferator activated receptor ${\gamma}$ ($PPAR{\gamma}$). The expression of FAS and LPL, which are terminal differentiation markers of mature adipocytes, was also reduced in the 3T3-L1 adipocytes treated with dichloromethane fractions from I. verum Hooker fil. In addition, the treatment significantly inhibited mitotic clonal expansion, which is essential for adipocyte differentiation, by arresting the G1 phase of the cell cycle. Taken together, these results suggest that dichloromethane fractions from I. verum Hooker fil. may be a natural material with antiobesity effects.

Purification and Characterization of Anticarcinogenic Compound from Corni fructus (산수유에 함유된 항암물질의 정제 및 특성)

  • Kim, Byeong-Hyeon;Park, Kyung-Wuk;Kim, Jae-Yong;Jeong, Ill-Yun;Yang, Gi-Ho;Cho, Young-Sook;Yee, Sung-Tae;Seo, Kwon-Il
    • Korean Journal of Food Science and Technology
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    • v.36 no.6
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    • pp.1001-1007
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    • 2004
  • Chloroform layer from methanol extract of Corni fructus (Cornaceae) showed strong antiproliferation effect on human cancer cell lines by SRB assay. Anticarcinogenic-active compound was isolated and purified by silica gel column and thin layer chromatograpies, and identified as ursolic acid ($3{\beta}$-hydroxyrus-12-ene-28-oic acid, MW:456) by mass and IR spectrophotometries, and $^1H-and\;^{13}C-NMRs$. The compound inhibited proliferation of A549 (human lung cancer cell line) and MCF-7 (human breast cancer cell line) cells in dose-dependant manner when treated for 48 hr. Inhibition rates of both cells were over 40% and 90% compared with control cells at the $30\;{\mu}g/mL\;and\;100\;{\mu}g/mL$, respectively. Morphology of cells treated with the compound for 15 hr at $10\;{\mu}g/mL$ was distorted with shrinked cell mass, and cell number was lower than that of control cells. Cell cycle analysis showed sub-G1 phase arrest in both cell lines following 15 hr exposure to the compound; % of cell phase increased to 11.7 and 11.2% compared to the control of 4.0% and 2.1% in A549 and MCP-7 cells, respectively.

Knocking Down Nucleolin Expression Enhances the Radiosensitivity of Non-Small Cell Lung Cancer by Influencing DNA-PKcs Activity

  • Xu, Jian-Yu;Lu, Shan;Xu, Xiang-Ying;Hu, Song-Liu;Li, Bin;Qi, Rui-Xue;Chen, Lin;Chang, Joe Y.
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.8
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    • pp.3301-3306
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    • 2015
  • Nucleolin (C23) is an important anti-apoptotic protein that is ubiquitously expressed in exponentially growing eukaryotic cells. In order to understand the impact of C23 in radiation therapy, we attempted to investigate the relationship of C23 expression with the radiosensitivity of human non-small cell lung cancer (NSCLC) cells. We investigated the role of C23 in activating the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs), which is a critical protein for DNA double-strand breaks (DSBs) repair. As a result, we found that the expression of C23 was negatively correlated with the radiosensitivity of NSCLC cell lines. In vitro clonogenic survival assays revealed that C23 knockdown increased the radiosensitivity of a human lung adenocarcinoma cell line, potentially through the promotion of radiation-induced apoptosis and adjusting the cell cycle to a more radiosensitive stage. Immunofluorescence data revealed an increasing quantity of ${gamma}$-H2AX foci and decreasing radiation-induced DNA damage repair following knockdown of C23. To further clarify the mechanism of C23 in DNA DSBs repair, we detected the expression of DNA-PKcs and C23 proteins in NSCLC cell lines. C23 might participate in DNA DSBs repair for the reason that the expression of DNA-PKcs decreased at 30, 60, 120 and 360 minutes after irradiation in C23 knockdown cells. Especially, the activity of DNA-PKcs phosphorylation sites at the S2056 and T2609 was significantly suppressed. Therefore we concluded that C23 knockdown can inhibit DNA-PKcs phosphorylation activity at the S2056 and T2609 sites, thus reducing the radiation damage repair and increasing the radiosensitivity of NSCLC cells. Taken together, the inhibition of C23 expression was shown to increase the radiosensitivity of NSCLC cells, as implied by the relevance to the notably decreased DNA-PKcs phosphorylation activity at the S2056 and T2609 clusters. Further research on targeted C23 treatment may promote effectiveness of radiotherapy and provide new targets for NSCLC patients.

An Experimental Study on Apoptosis of Cultivated Wild Ginseng Distilled Herbal Acupuncture by controlled pH and Electrolyte (pH 및 전해질 조절 산양산삼(山養山蔘) 증류약침(蒸溜藥鍼)의 Apoptosis에 관(關)한 실험적(實驗的) 연구(硏究))

  • Chu, Ching sheng;Lee, Sun-gu;Kwon, Ki-rok
    • Journal of Acupuncture Research
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    • v.21 no.6
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    • pp.1-17
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    • 2004
  • Objective : To compare and examine how adjustment of pH and electrolyte can affect the efficacy of cultivated wild ginseng distilled herbal acupuncture, we've administered pure cultivated wild ginseng distilled herbal acupuncture and pH and electrolyte adjusted cultivated wild ginseng distilled herbal acupuncture on A549 human lung cancer lines. Then mRNA and proteins which take parts in apoptosis were examined. Methods : Pure cultivated wild ginseng distilled herbal acupuncture treated group was set as the control group and pH and electrolyte adjusted cultivated wild ginseng distilled herbal acupuncture groups were administered on A549 human lung cancer lines. Cell toxicity was carefully examined and from the analysis of DNA fragmentation, RT-PCR, and Western blot, manifestation of mRNA and proteins which are associated with apoptosis were inspected. Results : The following results were obtained on apoptosis of A549 human lung cancer lines after administering pH and electrolyte adjusted cultivated wild ginseng distilled herbal acupuncture. 1. Measuring cell toxicity of lung cancer cells, higher cell toxicity was detected at pH and electrolyte adjusted groups and the results were concentration dependent. 2. Through DNA fragmentation, we were able to confirm cell destruction in all groups. 3. Experiment groups treated with cultivated wild ginseng distilled herbal acupuncture showed inhibition of Bcl-2 and COX-2 at mRNA and Protein level, whileas increase of Bax was shown. 4. Manifestation of p21, p53, Cyclin E, and Cyclin D1 were confirmed in all groups. 5. Extrication of Cytochrome C was detected at all groups, as well as increased activity of the enzyme caspase-3 and caspase-9, and PARP fragmentation were confirmed. Conclusions : From the above results, we can carefully deduce cell destruction of A549 human lung cancer lines were induced by Apoptosis. At the same concentration level, cell destruction efficacy was better with adjusted pH and electrolyte. Cultivated wild ginseng distilled herbal acupuncture also showed decrease of Bcl-2 and COX-2, as well as increase of Bax. Since cultivated wild ginseng distilled herbal acupuncture increases manifestation of p21, p53, Cyclin E, and Cyclin D1, it affects cellular cycle and through these phenomena, we can consider extrication of Cytochrome C, increase of caspase, and PARP fragmentation are the results.

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Anti-proliferation, Cell Cycle Arrest, and Apoptosis Induced by Natural Liquiritigenin from Licorice Root in Oral Squamous Cell Carcinoma Cells (구강편평세포암종 세포에서 감초 유래 Liquiritigenin의 항증식, 세포주기 정지 및 세포사멸 유도)

  • Kwak, Ah-Won;Yoon, Goo;Chae, Jung-Il;Shim, Jung-Hyun
    • Journal of Life Science
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    • v.29 no.3
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    • pp.295-302
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    • 2019
  • Liquiritigenin (LG) is a chiral flavonoid isolated from the roots of licorice. It exhibits multiple biological activities including anti-oxidant, anti-cancer, and anti-inflammatory effects. In particular though, the anti-cancer activity of LG in oral squamous cell carcinoma has yet to be elucidated, and LG-induced apoptosis in oral squamous cell carcinoma remains poorly understood. In the present study, we tested the role of LG in inducing apoptosis in oral squamous cell carcinoma cells. LG treatment of HN22 cells resulted in a dose-dependent inhibition of cell viability as detected by a 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide assay. The induction of apoptosis in terms of Annexin V/7-Aminoactinomycin D staining, sub-G1 population, and multi-caspase activity were assessed with a $Muse^{TM}$ Cell Analyzer. Flow cytometric analysis revealed that LG treatment resulted in G2/M arrest in cell cycle progression and downregulation of cyclin B1 and CDC2 expression in a concentration-dependent manner. It also resulted in significant upregulation of p27. In addition, LG was seen to trigger the generation of reactive oxygen species and induce CCAAT/enhancer-binding protein homologous protein and 78-kDa glucose-regulated protein in concentration-dependent upregulation. The LG treatment of HN22 cells led to a loss of mitochondrial membrane potential (${\Delta}{\Psi}m$); it also reduced the levels of anti-apoptotic protein and increased the expression of apoptotic protease activating factor-1, cleaved poly (ADP-ribose)polymerase and Bax. Overall, our results indicate that the pro-apoptotic effects of LG in HN22 cells depend on the activation of both intrinsic and extrinsic signaling pathways. Thus, our results suggest that LG constitutes a natural compound with a potential role as an anti-tumor agent in oral squamous cell carcinoma.