• Title/Summary/Keyword: cancer cell growth inhibition

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Different Immunology Mechanisms of Phellinus igniarius in Inhibiting Growth of Liver Cancer and Melanoma Cells

  • Zhou, Cui;Jiang, Song-Song;Wang, Cui-Yan;Li, Rong;Che, Hui-Lian
    • 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.

New HDAC inhibitor, IN2001 induces apoptosis/cell cycle arrest in human breast cancer cells

  • Joung, Ki-Eun;Min, Kyung-Nan;Cho, Min-Jung;An, Jin-Young;Kim, Dae-Ki;Sheen, Yhun-Yhong
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2003.11a
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    • pp.90-90
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    • 2003
  • The acetylation of histone is one of the mechanisms involved in the regulation of gene expression and is tightly controlled by two core enzymes, histone acetyltransferase (HAT) and deacetylase (HDAC). There are several reports that imbalance of HAT and HDAC activity is associated with abnormal behavior of the cells in morphology, cell cycle, differentiation, and carcinogenesis. Recently, an increasing number of structurally diverse HDAC inhibitors have been identified that inhibit proliferation and induce differentiation and/or apoptosis of tumor cells in vivo and in vitro. In this study, we have investigated the effects of novel HDAC inhibitors, IN2001 on ER positive and ER negative human breast cancer cell lines. The growth inhibition, cell cycle arrest and apoptosis of cells by HDAC inhibitors were determined using SRB assay, DNA fragmentation, and flow cytometry. We found that IN 2001 as well as Trichostatin A inhibited cell growth dose-dependently in both ER positive and ER negative human breast cancer cell lines. The growth inhibition with HDAC inhibitors was associated with profound morphological change. The result of cell cycle analysis after 24 h exposure of IN2001 showed G2-M cell cycle arrest in MCF-7 cell and apoptosis in T47D and MDA-MB-231 cell. In summary, IN2001 has antiproliferative effect on human breast cancer cells regardless of the expression of estrogen receptor. These findings heights the possibility of developing HDAC inhibitors as potential anticancer therapeutic agents for the treatment of breast cancer.

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New HDAC inhibitor, IN2001 induces apoptosis/cell cycle arrest in human breast cancer cells

  • Euno, Joung-Ki;Nan, Min-Kyung;Jung, Cho-Min;Young, An-Jin;Kim, -Dae-Ki;Yhong, Sheen-Yhun
    • Proceedings of the Korea Society of Environmental Toocicology Conference
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    • 2003.10a
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    • pp.180-180
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    • 2003
  • The acetylation of histone is one of the mechanisms involved in the regulation of gene expression and is tightly controlled by two core enzymes, histone acetyltransferase (HAT) and deacetylase (HDAC). There are several reports that imbalance of HAT and HDAC activity is associated with abnormal behavior of the cells in morphology, cell cycle, differentiation, and carcinogenesis. Recently, an increasing number of structurally diverse HDAC inhibitors have been identified that inhibit proliferation and induce differentiation and/or apoptosis of tumor cells in vivo and in vitro. In this study, we have investigated the effects of novel HDAC inhibitors, IN2001 on ER positive and ER negative human breast cancer cell lines. The growth inhibition, cell cycle arrest and apoptosis of cells by HDAC inhibitors were determined using SRB assay, DNA fragmentation, and flow cytometry. We found that IN 2001 as well as Trichostatin A inhibited cell growth dose-dependently in both ER Positive and ER negative human breast cancer cell lines. The growth inhibition with HDAC inhibitors was associated with profound morphological change. The result of cell cycle analysis after 24 h exposure of IN2001 showed G2-M cell cycle arrest in MCF-7 cell and apoptosis in T47B and MDA-MB-231 cell. In summary, IN2001 has antiproliferative effect on human breast cancer cells regardless of the expression of estrogen receptor. These findings heights the possibility of developing HDAC inhibitors as potential anticancer therapeutic agents for the treatment of breast cancer.

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Tumour Suppressive Effects of WEE1 Gene Silencing in Breast Cancer Cells

  • Ghiasi, Naghmeh;Habibagahi, Mojtaba;Rosli, Rozita;Ghaderi, Abbas;Yusoff, Khatijah;Hosseini, Ahmad;Abdullah, Syahrilnizam;Jaberipour, Mansooreh
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.11
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    • pp.6605-6611
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    • 2013
  • Background: WEE1 is a G2/M checkpoint regulator protein. Various studies have indicated that WEE1 could be a good target for cancer therapy. The main aim of this study was to asssess the tumor suppressive potential of WEE1 silencing in two different breast cancer cell lines, MCF7 which carries the wild-type p53 and MDA-MB468 which contains a mutant type. Materials and Methods: After WEE1 knockdown with specific shRNAs downstream effects on cell viability and cell cycle progression were determined using MTT and flow cytometry analyses, respectively. Real-time PCR and Western blotting were conducted to assess the effect of WEE1 inhibition on the expression of apoptotic (p53) and anti-apoptotic (Bcl2) factors and also a growth marker (VEGF). Results: The results showed that WEE1 inhibition could cause a significant decrease in the viability of both MCF7 and MDA-MB-468 breast cancer cell lines by more than 50%. Interestingly, DNA content assays showed a significant increase in apoptotic cells following WEE1 silencing. WEE1 inhibition also induced upregulation of the apoptotic marker, p53, in breast cancer cells. A significant decrease in the expression of VEGF and Bcl-2 was observed following WEE1 inhibition in both cell lines. Conclusions: In concordance with previous studies, our data showed that WEE1 inhibition could induce G2 arrest abrogation and consequent cell death in breast cancer cells. Moreover, in this study, the observed interactions between the pro- and anti-apoptotic proteins and decrease in the angiogenesis marker expression confirm the susceptibility to apoptosis and validate the tumor suppressive effect of WEE1 inhibition in breast cancer cells. Interestingly, the levels of the sensitivity to WEE1 silencing in breast cancer cells, MCF7 and MDA-MB468, seem to be in concordance with the level of p53 expression.

Effect of Snake Venom Toxin on Inhibition of Colorectal Cancer HT29 Cells Growth via Death Receptors Mediated Apoptosis

  • Shim, Yoon Seop;Song, Ho Sueb
    • Journal of Acupuncture Research
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    • v.31 no.2
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    • pp.87-98
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    • 2014
  • Objectives : We investigated whether snake venom toxin(SVT) from Vipera lebetina turanica sensitizes HT29 human epithelial colorectal cancer cells to tumor necrosis factor(TNF)-related apoptosis-inducing ligand(TRAIL) induced apoptosis in cancer cells. Methods : Cell viability assay was used to assess the inhibitory effect of TRAIL on cell growth of HT29 human colorectal cancer cells. And 6-diamidino-2-phenylindole(DAPI), terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay(TUNEL) staining assay were used to evaluate cell-apoptosis. Western blot analysis were conducted to observe apoptosis related proteins and death receptor. To assess whether the synergized inhibitory effect of SVT and TRAIL on reactive oxygen species(ROS) generation was reversed by strong anti-oxidative agent. Results : SVT with TRAIL inhibited HT29 cell growth different from TRAIL alone. Consistent with cell growth inhibition, the expression of TRAIL receptors; Expression of death receptor(DR)4 and DR5 was significantly increased and intrinsic pro-apoptotic cleaved caspase-3, -9 was subsequently increased together with increase of Bax/Bcl-2 ratio and extrinsic pro-apototic caspase-8 was also activated. In addition, the expression of anti-apoptotic survival proteins, a marker of TRAIL resistance(eg, cFLIP, survivin, X-linked inhibitor of apoptosis protein(XIAP) and Bcl-2) was suppressed by the combination treatment of SVT and TRAIL. Pretreatment with the ROS scavenger N-acetylcysteine abolished the SVT and TRAIL-induced upregulation of DR4 and DR5 expression and expression of the intrinsic pro-apoptotic caspase-3 and-9. Conclusion : The collective results suggest that SVT facilitates TRAIL-induced apoptosis in $HT_{29}$ human epithelial colorectal cancer cells through up-regulation of the TRAIL receptors; DR4 and DR5 and consecutive induction of bilateral apoptosis via regulating apoptosis related proteins.

Effect of β-carotene on Cell Growth Inhibition of KB Human Oral Cancer Cells

  • Yang, Sung-Su;Kim, Su-Gwan;Park, Byung-Sun;Go, Dae-San;Yu, Sun-Kyoung;Kim, Chun Sung;Kim, Jeongsun;Kim, Do Kyung
    • International Journal of Oral Biology
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    • v.41 no.3
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    • pp.105-111
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    • 2016
  • ${\beta}-carotene$ is present in carrots, pumpkins, and sweet potatoes. It suppresses many types of cancers by regulating cellular proliferation and apoptosis through a variety of mechanisms. However, the effects of ${\beta}-carotene$ on oral cancer cells have not been clearly established. The main goal of this study was to investigate the effects of ${\beta}-carotene$ on cell growth and apoptosis in oral cancer cells. Our results demonstrate that treatment with ${\beta}-carotene$ induced inhibition of cell growth, and that the effect was dependent on ${\beta}-carotene$ treatment time and concentration in KB cells. Furthermore, treatment with ${\beta}-carotene$ induced nuclear condensation and fragmentation in KB cells. ${\beta}-carotene$ promoted proteolytic cleavage of procaspase-3, -7, -8 and -9 with associated increases in the concentration of cleaved caspase-3, -7, -8 and -9. In addition, the level of cleaved PARP was increased by ${\beta}-carotene$ treatment in KB cells. These results suggest that ${\beta}-carotene$ can suppress cell growth and induce apoptosis in KB human oral cancer cells, and that it may have potential usefulness in anti-cancer drug discovery efforts.

Evaluation of antioxidant and cancer cell growth inhibition activities of red rice and black rice (적미와 흑미의 항산화 활성 및 암세포성장 억제 효과)

  • Kim, Hye Won;Oh, Sea Kwan;Lee, Jeong Heui;Yoon, Mi Ra;Kim, Dae Jung;Choi, Im Soo;Kim, Jung Gon;Lee, Jeom Sig
    • Food Science and Preservation
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    • v.20 no.6
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    • pp.834-839
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    • 2013
  • The extraction yield, total phenolics content, antioxidant activity, cancer cell growth inhibition (A549 and MCF 7), and lung cancer cell (A549) viability of red rice and black rice were investigated, to evaluate the functional properties of colored rice. The extraction yields and the total phenolics contents of the rice cultivars were Heugseol > Heugkwang > Hongjinju > Jeogjinju > Ilpum. Also, the DPPH radical scavenging activity of the black rice did not differ from that of the red rice, whereas its activity among its cultivars was Jeogjinju > Heugseol > Heugkwang > Hongjinju > Ilpum. The ABTS antioxidant activity of the black rice (Heugkwang, Heugseol) was greater than that of the red rice. The total phenolics was partly attributed to its high antioxidant. On the other hand, the effect of the red rice on the lung cancer cell (A549) viability was higher than that of the black rice. The breast cancer cell (MCF 7) growth inhibition activity of the black rice did not differ from that of the red rice. Our results indicate that the ABTS antioxidant activity of black rice is better than that of red rice, and the lung cancer cell (A549) viability of red rice is better than that of black rice.

Antiproliferative Activity of Convergence of Vegetable Extract in Cancer cells (야채추출물의 융복합적 암세포 증식 억제효과)

  • Park, Hae-Ran;Park, Jeong-Sook
    • Journal of Digital Convergence
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    • v.14 no.1
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    • pp.491-496
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    • 2016
  • The present sturdy was designed to determine the effect of the antiproliferation in human cancer cells, using vegetable extract of Radish, Radish leaves, Burdock, Shiitake, Carrot of the ordinary vegetable soup. Human cancer cells identify the cancer cell growth with MTS, using stomach cancer cell line (AGS), human promyelocytic leukemia (HL-60) and lung cancer cell line (A549). Shiitake and Carrot are effective on the cancer cell growth inhibition activities of AGS. Radish leaves, Burdock, Carrot have a significance with HL-60 and Radish, Radish leaves works well in A549. The vegetable extracts which is effective for cancer cell growth inhibition is considered to applicate base line data for using functional materials and for wellness life.

Inhibitory Activity of Brine Mineral Water on Cancer Cell Growth, Metastasis and Angiogenesis (해양성 광천수의 암세포 성장, 전이 및 신생 혈관 생성 억제 효과)

  • Kim, Wan-Jae;Li, Hua;Yoon, Taek-Joon;Sim, Jae-Man;Choi, Seon-Kang;Lee, Kwang-Ho
    • The Korean Journal of Food And Nutrition
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    • v.22 no.4
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    • pp.542-547
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    • 2009
  • Brine mineral water(BMW) has recently gained attention as a new water resource due to its biological activities. In this study, BMW from the Geumjin area(Gangneung-city, Korea) was evaluated for its growth inhibition, anti-metastasis and anti-angiogenesis activity against cancer cells. The in vitro cytotoxicity was measured by CCK assay, and the anti-metastasis activity was estimated by lung metastasis in vivo. The in vitro incubation of mouse splenic cells with BMW that had been diluted more than 4-fold showed no effect on the cell growth when compared to a control group. Additionally, BMW inhibited the growth of the EL-4, L5178Y-R and colon26-M3.1 cancer cell lines in a dose-dependent manner. In vivo evaluation of the anti-metastasis activity of BMW in BALB/c mice inoculated with the colon26-M3.1 cell line revealed dose-dependent inhibition in response to treatment with samples that were diluted by up to 9 times. Finally, treatment with BMW effectively suppressed the growth of vascular endothelial growth factor(VEGF) added human umbilical vein endothelial cells. Overall, these results suggest that BMW has anti-cancer activity.

Effect of respiratory syncytial virus on the growth of hepatocellular carcinoma cell-lines

  • Choi, Song Hee;Park, Byoung Kwon;Lee, Keun-Wook;Chang, Jun;Lee, Younghee;Kwon, Hyung-Joo
    • BMB Reports
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    • v.48 no.10
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    • pp.565-570
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    • 2015
  • In several reports, the respiratory syncytial virus (RSV) was identified as an oncolytic virus in cancer cells (e.g., lung and prostate cancer). However, the effects of RSV in hepatocellular carcinoma (HCC) cells have not yet been investigated. Here, we observed the inhibitory effects of RSV infection in HCC cell-lines. Cell growth was significantly decreased by RSV infection in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. After RSV infection, plaque formation and syncytial formation were observed in affected Hep3B and Huh-7 cells. RSV protein-expression was also detected in Hep3B and Huh-7 cells; however, only Huh-7 cells showed apoptosis after RSV infection. Furthermore, inhibition of cell migration by RSV infection was observed in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. Therefore, further investigation is required to clarify the molecular mechanism of RSV-mediated inhibition of HCC cell growth, and to develop potential RSV oncolytic viro-therapeutics.