gd3 synthase overexpression sensitizes hepatocarcinoma cells to hypoxia and reduces tumor growth by suppressing the csrcnf-κb survival pathwaygd3合酶过度糖分会让肝癌细胞缺氧,降低肿瘤的生长通过抑制csrcnf-κb生存途径.pdfVIP

gd3 synthase overexpression sensitizes hepatocarcinoma cells to hypoxia and reduces tumor growth by suppressing the csrcnf-κb survival pathwaygd3合酶过度糖分会让肝癌细胞缺氧,降低肿瘤的生长通过抑制csrcnf-κb生存途径.pdf

  1. 1、有哪些信誉好的足球投注网站(book118)网站文档一经付费(服务费),不意味着购买了该文档的版权,仅供个人/单位学习、研究之用,不得用于商业用途,未经授权,严禁复制、发行、汇编、翻译或者网络传播等,侵权必究。。
  2. 2、本站所有内容均由合作方或网友上传,本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺!文档内容仅供研究参考,付费前请自行鉴别。如您付费,意味着您自己接受本站规则且自行承担风险,本站不退款、不进行额外附加服务;查看《如何避免下载的几个坑》。如果您已付费下载过本站文档,您可以点击 这里二次下载
  3. 3、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等,请点击“版权申诉”(推荐),也可以打举报电话:400-050-0827(电话支持时间:9:00-18:30)。
  4. 4、该文档为VIP文档,如果想要下载,成为VIP会员后,下载免费。
  5. 5、成为VIP后,下载本文档将扣除1次下载权益。下载后,不支持退款、换文档。如有疑问请联系我们
  6. 6、成为VIP后,您将拥有八大权益,权益包括:VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
  7. 7、VIP文档为合作方或网友上传,每下载1次, 网站将根据用户上传文档的质量评分、类型等,对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档
查看更多
gd3 synthase overexpression sensitizes hepatocarcinoma cells to hypoxia and reduces tumor growth by suppressing the csrcnf-κb survival pathwaygd3合酶过度糖分会让肝癌细胞缺氧,降低肿瘤的生长通过抑制csrcnf-κb生存途径

GD3 Synthase Overexpression Sensitizes Hepatocarcinoma Cells to Hypoxia and Reduces Tumor Growth by Suppressing the cSrc/NF-kB Survival Pathway 1,2 1 1 ´ 1 2 Josep M. Lluis , Laura Llacuna , Claudia von Montfort , Cristina Barcena , Carlos Enrich , Albert 1. ´ 1,3. Morales *, Jose C. Fernandez-Checa * 1 Department of Cell Death and Proliferation, IIBB-CSIC, and Liver Unit, Hospital Clinic, IDIBAPS-CIBEK, CIBEREHD, Barcelona, Spain, 2 Departament de Biologia Cellular, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain, 3 Research Center for Alcoholic Liver and Pancreatic Diseases, Keck School of Medicine of the University of Southern California, Los Angeles, California, United States of America Abstract Background: Hypoxia-mediated HIF-1a stabilization and NF-kB activation play a key role in carcinogenesis by fostering cancer cell survival, angiogenesis and tumor invasion. Gangliosides are integral components of biological membranes with an increasingly recognized role as signaling intermediates. In particular, ganglioside GD3 has been characterized as a proapoptotic lipid effector by promoting cell death signaling and suppression of survival pathways. Thus, our aim was to analyze the role of GD3 in hypoxia susceptibility of hepatocarcinoma cells and in vivo tumor growth. Methodology/Principal Findings: We generated and characterized a human hepatocarcinoma cell line stably expressing GD3 synthase (Hep3B-GD3), which catalyzes the synthesis of GD3 from GM3. Despite increased GD3 levels (2–3 fold), no significant changes in cell morphology or growth were observed in Hep3B-GD3 cells compared to wild type Hep3B cells under normoxia.

您可能关注的文档

文档评论(0)

hello118 + 关注
实名认证
文档贡献者

该用户很懒,什么也没介绍

1亿VIP精品文档

相关文档