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Neoplasma
Article
Data sources: UnpayWall
Neoplasma
Article . 2012 . Peer-reviewed
Data sources: Crossref
Neoplasma
Article . 2012
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Overexpression of ECM1 Contributes to Migration and Invasion in Cholangiocarcinoma Cell

Authors: G P, Xiong; J X, Zhang; S P, Gu; Y B, Wu; J F, Liu;

Overexpression of ECM1 Contributes to Migration and Invasion in Cholangiocarcinoma Cell

Abstract

Although the expression of extracellular matrix protein-1 (ECM1) has been documented in several tumor models, the function of ECM1 has remained unclear. In this study, expression of ECM1 was detected by real time PCR and immunohistochemistry. The role and mechanism of ECM1 overexpression in cholangiocarcinoma (CCA) cells were assessed by wound-healing, matrigel invasion assay and Western blotting. Expression of ECM1 was significantly elevated in CCA tissues than that in adjacent noncancerous, cholangitis and normal bile duct tissues. Its overexpression was associated with poor differentiation, lymph node metastasis, poor prognosis, and the level of CA199, MMP-9, estrogen receptor. Knockdown of ECM1 suppressed migration and invasion of CCA cells. Using PI3K or IKK inhibitor reduced the level of phospho-Akt or phospho-IκBα as well as ECM1. Taken together, overexpression of ECM1 may contribute to CCA initiation and progression through promoting migration and invasion of CCA cells, its overexpression was associated with Akt/NF-κB signaling axis.

Related Organizations
Keywords

Male, Extracellular Matrix Proteins, Blotting, Western, NF-kappa B, Apoptosis, Middle Aged, Real-Time Polymerase Chain Reaction, Cholangiocarcinoma, Immunoenzyme Techniques, Phosphatidylinositol 3-Kinases, Bile Ducts, Intrahepatic, Bile Duct Neoplasms, Cell Movement, Cell Adhesion, Humans, Female, Neoplasm Invasiveness, RNA, Messenger, Proto-Oncogene Proteins c-akt, Cell Proliferation

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    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    38
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
38
Top 10%
Top 10%
Top 10%
bronze
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