中国药学杂志
    
           首页  |  期刊介绍  |  编 委 会  |  投稿指南  |  期刊订阅  |  广告服务  |  会议信息  |  联系我们  | 
�й�ҩѧ��־ 2011, Vol. 46 Issue (23) :1805-1810    DOI:
���� ����Ŀ¼ | ����Ŀ¼ | ������� | �߼����� << | >>
������������ö�kallistatin������ǿ���о�
�����ȣ����£���ӱ�ۣ����з�������ǿ������*
���ȴ�ѧ����ҩ��ѧ�о���������ҩ������������о����ģ����� Ȫ�� 362021
WANG Qi-zhao�� DIAO Yong�� L�� Ying-hui�� LI Zhao-fa�� WANG Li-qiang�� XU Rui-an*
Institute of Molecular Medicine�� Huaqiao University�� Molecular Medicine Engineering Research Center�� Ministry of Education�� Quanzhou 362021�� China

Download: PDF (2023KB)   HTML (0KB)   Export: BibTeX or EndNote (RIS)      Supporting Info
ժҪ Ŀ�� ��ǿkallistatin(Kal)��һ�๦����Դ�Կ�Ѫ���������ӿ��������ԡ����� ���������������Kal����Ӧ�ã�����֬���彫����Ŀ�����������תȾ����Ƥϸ��������ϸ��������������������ƶ�ϸ�����Ե�Ӱ�졣��� Kal�Էΰ�ϸ��A549��NCI-H446��SPC-A1�����������á�Kal��Trail��vasostatin(Vas)���ϣ��ɼ�ǿ��SPC-A1ϸ�����������ã����������ϸ��������ò�δ��һ����ǿ��Kal��angiostatin(Ang)��Vas ����Ӧ�ÿ�������ǿ��Ѫ����Ƥϸ��EVC304������Ǩ���Լ�С���γɵ��������á����� Kal�������������͵Ļ����������ã���ǿ������ϸ����Ѫ����Ƥϸ�����������ã�Ϊ�����Ķ�������������ṩ��ʵ�������
Service
�ѱ����Ƽ�������
�����ҵ����
�������ù�����
Email Alert
RSS
�����������
������
����
��ӱ��
���з�
����ǿ
����*
������
����
��ӱ��
���з�
����ǿ
����*
�ؼ����� kallistatin   ��Ѫ���γ�   �ΰ�   ��������   �ǰ�������     
Abstract�� OBJECTIVE Kallistatin (Kal) is a new endogenous anti-angiogenic factor. It also has a role in anti-inflammation and anti-oxidation. Moreover�� it could directly inhibit the proliferation of cancer cells. The aim of this study is to enhance the activities of this multi-functional gene. METHODS Kal together with other genes was co-transfected into cells using lipofectamine 2000 (Lipo)�� and the cell activities were measured via MTT�� scratch�� transwell and tube formation assays. RESULTS It was found that Kal could inhibit the growth of A549�� NCI-H446 and SPC-A1 cells in vitro. The combination of Kal with Trail or vasostatin(Vas) improved the growth inhibitive effect on SPC-A1 cells�� but the combination of these three genes failed to further enhance this phenomenon. Moreover�� combination of Kal with angiostatin (Ang) or Vas�� two other anti-angiogenic factors�� enhanced the anti-cancer and anti-angiogenic activities of Kal for EVC304 cells. The combination of the three genes had the most significant activities. CONCLUSION The activities of Kal can be enhanced by using multigene co-transfenction. This study has provided valuable experimental data for the further application of cancer multigene therapy.
Keywords�� kallistatin,   anti-angiogenesis,   lung cancer,   gene therapy,   non-oncogene addiction     
�ո�����: 2011-11-11;
���ñ���:   
������, ����, ��ӱ�۵� .������������ö�kallistatin������ǿ���о�[J]  �й�ҩѧ��־, 2011,V46(23): 1805-1810
WANG Qi-zhao, DIAO Yong, L�z Ying-hui etc .Enhancing the Anti-Cancer Activities of Kallistatin via Multigene Co-Transfection[J]  Chinese Pharmaceutical Journal, 2011,V46(23): 1805-1810
��
[1] CHAO J�� CHAI K X�� CHEN L M�� et al. Purification�� characterization�� and distribution in normotensive and spontaneously hypertensive rats[J]. J Biol Chem�� 1990�� 265(27)�� 16394-16401. [2] ZHOU G X�� CHAO L�� CHAO J. Kallistatin�� a novel human tissue kallikrein inhibitor. In�� Purification�� characterization�� and reactive center sequence[J]. J Biol Chem�� 1992�� 267(36)�� 25873-25880. [3] MIAO R Q�� AGATA J�� CHAO L�� et al. Kallistatin is a new inhibitor of angiogenesis and tumor growth[J]. Blood�� 2002�� 100(9)�� 3245-3252. [4] MIAO R Q�� CHEN V�� CHAO L�� et al. Structural elements of kallistatin required for inhibition of angiogenesis[J]. Am J Physiol Cell Physiol�� 284(6)�� 1604-1613. [5] DIAO Y�� MA J�� XIAO W�� et al. Inhibition of angiogenesis and HCT-116 xenograft tumor growth in mice by kallistatin[J]. World J Gastroenterol�� 2007�� 13(34)�� 4615-4619. [6] TSE L Y�� SUN X�� JIANG H�� et al. Adeno-associated virus-mediated expression of kallistatin suppresses local and remote hepatocellular carcinomas[J]. J Gene Med�� 2008�� 10(5)�� 508-517. [7] DEVANI M�� VECCHI M�� FERRERO S�� et al. Kallikrein-kinin system in inflammatory bowel diseases�� Intestinal involvement and correlation with the degree of tissue inflammation[J]. Dig Liver Dis�� 2005�� 37(9)�� 665-673. [8] WANG C R�� CHEN S Y�� WU C L�� et al. Prophylactic adenovirus-mediated human kallistatin gene therapy suppresses rat arthritis by inhibiting angiogenesis and inflammation[J]. Arthritis Rheum�� 52(4)�� 1319-1324. [9] CHAO J�� YIN H�� YAO Y Y�� et al. Novel role of kallistatin in protection against myocardial ischemia-reperfusion injury by preventing apoptosis and inflammation[J]. Hum Gene Ther�� 2006�� 17(12)�� 1201-1213. [10] SHEN B�� HAGIWARA M�� YAO Y Y�� et al. Salutary effect of kallistatin in salt-induced renal injury�� inflammation�� and fibrosis via antioxidative stress[J]. Hypertension�� 2008�� 51(5)�� 1358-1365. [11] HSIEH J L�� SHEN P C�� SHIAU A L�� et al. Adenovirus-mediated kallistatin gene transfer ameliorates disease progression in a rat model of osteoarthritis induced by anterior cruciate ligament transection[J]. Hum Gene Ther�� 2009�� 20��2���� 147-158. [12] HUANG X�� WANG X�� DONG H�� et al. High level expression of recombinant human kallistatin in Pichia pastoris and its bioactivity[J]. Chin J Biotech(���﹤��ѧ��)�� 2010�� 26(2)�� 249-255. [13] JIANG X�� LI H�� QIAO H�� et al. Combining kallistatin gene therapy and meloxicam to treat hepatocellular carcinoma in mice[J]. Cancer Sci�� 2009�� 100(11)�� 2226-2233. [14] SUN X�� KRISSANSEN G W�� FUNG P W C�� et al. Anti-angiogenic therapy subsequent to adeno-associated-virus-mediated immunotherapy eradicates lymphomas that disseminate to the liver[J]. Int J Cancer�� 2005�� 113(4)�� 670-677. [15] JIANG H�� MENG Q�� TAN H�� et al. Antiangiogenic therapy enhances the efficacy of transcatheter arterial embolization for hepatocellular carcinomas[J]. Int J Cancer�� 2007�� 121(2)�� 416-424. [16] SUN X�� QIAO H�� JIANG H�� et al. Intramuscular delivery of antiangiogenic genes suppresses secondary metastases after removal of primary tumors[J]. Cancer Gene Ther�� 2005�� 12(1)��35-45. [17] XU R�� SUN X�� TSE L Y�� et al. Long-term expression of angiostatin suppresses metastatic liver cancer in mice[J]. Hepatology�� 2003�� 37(6)��1451-1460. [18] YAO L��PIKE S E��PITTALUGA S��et al. Antitumor activities of the angiogenesis inhibitors interferon -inducible protein-10 and the calreticulin fragment vasostatin[J]. Cancer Immunol Immunother�� 2002�� 51(7)�� 358-366. [19] YAO L�� PIKE S E�� SETSUDA J�� et al. Effective targeting of tumor vasculature by the angiogenesis inhibitors vasostatin and interleukin-12[J]. Blood�� 2000�� 96�� 1900-1905. [20] CAI K X�� TSE L Y�� LEUNG C�� et al. Suppression of lung tumor growth and metastasis in mice by adeno-associated virus-mediated expression of vasostatin[J]. Clin Cancer Res�� 2008�� 14(3)�� 939-949. [21] DIAO Y�� MA J�� LI X�� et al. Construction and activity of recombinant adeno-associated virus expressing vasostatin[J]. Chin J Biotech(���﹤��ѧ��)�� 2008�� 24(11)�� 1949-1954. [22] FOLKMAN J. Angiogenesis�� an organizing principle for drug discovery[J]. Nat Rev Drug Discov�� 2007�� 6(4)�� 273-286. [23] SHI J�� ZHENG D�� MAN K�� et al. TRAIL�� a potential agent for cancer therapy[J]. Curr Mol Med�� 2003�� 3(8)�� 727-736. [24] SHI J�� ZHENG D�� LIU Y�� et al. Overexpression of soluble TRAIL induces apoptosis in human lung adenocarcinoma and inhibits growth of tumor xenografts in nude mice[J]. Cancer Res�� 2005�� 65(5)�� 1687-1692. [25] MA H�� LIU Y�� LIU S�� et al. Oral adeno-associated virus-sTRAIL gene therapy suppresses human hepatocellular carcinoma growth in mice[J]. Hepatology�� 2005�� 42(6)�� 1355-1363. [26] MA H�� LIU Y�� LIU S�� et al. Recombinant adeno-associated virus-mediated TRAIL gene therapy suppresses liver metastatic tumors[J]. Int J Cancer�� 2005�� 116(2)�� 314-321. [27] LUO J�� SOLIMINI N L�� ELLEDGE S J. Principles of cancer therapy�� oncogene and non-oncogene addiction[J]. Cell�� 2009�� 136(5)��823-837. Erratum in�� Cell�� 2009�� 138(4)��807. [28] SOLIMINI N L�� LUO J�� ELLEDGE S J. Non-oncogene addiction and the stress phenotype of cancer cells[J]. Cell�� 2007�� 130(6)�� 986-988. [29] WEINSTEIN I B�� JOE A. Oncogene addiction[J]. Cancer Res�� 2008�� 68��9���� 3076-3080.
[1] �������ᡤФ���ᣬ��ѧ��.ûʳ�Ӷ�����ûʳ��������С��Lewis�ΰ���ֳ�Լ�A549��Calu-3�ΰ���ֳ����������[J]. �й�ҩѧ��־, 2012,47(8): 585-589
[2] ������ �߿� ������ �԰�־ ���� ���� ��С�� ����־ �.����ע��rAAV2/rTNFR��Fc�Դ���ԭ�����ʪ�ؽ���ģ�͵���������[J]. �й�ҩѧ��־, 2011,46(7): 507-511
[3] ������ ������ ��� �μ��� ���� ���� ɣ����.��ҽҩ���Ʒ�Сϸ���ΰ��ľ��ü������������й����ݵ�ʵ֤[J]. �й�ҩѧ��־, 2011,46(4): 315-317
[4] ���� �ź� ��ѩ �򿡷� ������.�ɰ�ĵ�����յ��˷��ٰ�ϸ��A549����������Ƴ�̽[J]. �й�ҩѧ��־, 2011,46(24): 1890-1893
[5] �ᱣ�� ����ɺ ��ʥ�� .�׵��׽������ɼ���������ٰ��ͷ�Сϸ���ΰ��ٴ���Ч�۲�[J]. �й�ҩѧ��־, 2011,46(23): 1851-1854
[6] �߿� ��־�� ������ ���� ���� �ϻ� �Ĵ���.���鸴�������������������ϸ������ϸ������̼����ӵ������о�[J]. �й�ҩѧ��־, 2011,46(19): 1520-1525
[7] �ƾ��� ����ǿ.�Dz�������鵼�����ϸ�����Ϸ������о���չ[J]. �й�ҩѧ��־, 2011,46(18): 1381-1384
[8] �̱� ¦���� ���� ���ž� ���� ����ƽ.���ֶ��߻��Ʒ����������ڷ�Сϸ���ΰ���Ч�ıȽ�[J]. �й�ҩѧ��־, 2010,45(23): 1856-1858
[9] ��� �Ź��� �½� ���� ��ӯ ������.RRM1�����ڷ�Сϸ���ΰ���������Ѫ�еı�P��Լ�����������Ԥ�������[J]. �й�ҩѧ��־, 2010,45(23): 1847-1850
[10] ���� ������ ����.���鵰��HMGA2��������ҩ����°б�[J]. �й�ҩѧ��־, 2010,45(22): 1694-1700
[11] ������ �Ż�� �캣��.�зκϼ���С��Lewis�ΰ���ת�����ü���ػ��Ƶ�ʵ���о�[J]. �й�ҩѧ��־, 2010,45(22): 1729-1733
[12] ������ �Ź��� �½� ��� ����ΰ ������ũ �������� .RRM1��BRCA1�ı���뼪���������ϲ����������ڷ�Сϸ���ΰ����ٴ��о�[J]. �й�ҩѧ��־, 2010,45(20): 1577-1580
[13] ������;������;�̽�;��������.�����������й������Сϸ���ΰ��������ڵ�ҩ��ѧ�о�[J]. �й�ҩѧ��־, 2008,43(23): 1819-1822
[14] չ��;����Ӿ.RNA���ſ�������ȱ�ݲ�����Ⱦ�����ðе�[J]. �й�ҩѧ��־, 2008,43(16): 1201-1207
[15] ֣Ф��;������;½��ƽ;����;�½���.���ڻ������ƵĴ���֬����-DNA��������Ʊ����������[J]. �й�ҩѧ��־, 2008,43(13): 998-1002
Copyright 2010 by �й�ҩѧ��־