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CARMA3 is upregulated in human pancreatic carcinoma, and its depletion inhibits tumor proliferation, migration, and invasion
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  • 作者:Shiyu Du (1)
    Liping Jia (2)
    Yanli Zhang (1)
    Long Fang (1)
    Xiang Zhang (3)
    Yanhua Fan (1)
  • 关键词:CARMA3 ; Pancreatic cancer ; Proliferation ; NF ; κB
  • 刊名:Tumor Biology
  • 出版年:2014
  • 出版时间:June 2014
  • 年:2014
  • 卷:35
  • 期:6
  • 页码:5965-5970
  • 全文大小:
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  • 作者单位:Shiyu Du (1)
    Liping Jia (2)
    Yanli Zhang (1)
    Long Fang (1)
    Xiang Zhang (3)
    Yanhua Fan (1)

    1. Department of Gastroenterology, China-Japan Friendship Hospital, Chaoyang District, Beijing, 100029, China
    2. Department of Gastroscopy, Shenmu County Hospital, Guangming Road, Shenmu County, Shanxi, 719300, China
    3. Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, BCM600, Houston, TX, 77030, USA
  • ISSN:1423-0380
文摘
Elevated CARMA3 expression has been reported to be involved in tumor progression of several cancer types. In the present study, we examined the expression pattern of CARMA3 protein and its biological roles in human pancreatic carcinoma. Using immunohistochemistry, we checked CARMA3 protein expression in 95 pancreatic ductal carcinoma specimens. We found that CARMA3 was overexpressed in 34 of 95 (35.8?%) specimens. A significant association was observed between CARMA3 overexpression with histological grade (p--.0099) and nodal status (p--.0126). To further explore its biological roles, we knocked down CARMA3 expression in CAPAN2 cell line using small interfering RNA (siRNA). MTT growth assay, wound healing assay, and Transwell assay showed that CARMA3 depletion inhibited cell proliferation, migration, and invasion. We also showed that CARMA3 depletion inhibited EGF-induced nuclear factor-kappaB (NF-κB) activation and its target genes-expression. The effect of CARMA3 depletion on NF-κB signaling was significantly reduced in Bcl10-depleted cells. In conclusion, CARMA3 is overexpressed in pancreatic cancer and regulates malignant cell growth, invasion, and NF-κB signaling, which was dependent on its association with Bcl10.

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