Lipocalin 2 (LCN2) is a promising target for cholangiocarcinoma treatment and bile LCN2 level is a potential cholangiocarcinoma diagnostic marker
Cholangiocarcinoma (CCA) is a devastating disease due to resistance to traditional chemotherapies and radiotherapies. New therapeutic strategies against CCA are urgently needed. This study investigated the role of lipocalin-2 ( LCN2 ) in human cholangiocarcinoma as a potential therapeutic target and...
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Published in | Scientific reports Vol. 6; no. 1; p. 36138 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
26.10.2016
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
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Summary: | Cholangiocarcinoma (CCA) is a devastating disease due to resistance to traditional chemotherapies and radiotherapies. New therapeutic strategies against CCA are urgently needed. This study investigated the role of lipocalin-2 (
LCN2
) in human cholangiocarcinoma as a potential therapeutic target and diagnostic marker. So far, the role of
LCN2
in cancer is still controversial and studies regarding the role of LCN2 in CCA are limited.
LCN2
knockdown inhibited CCA cell growth
in vitro
and
in vivo
through induction of cell cycle arrest at G0/G1 phases and decreased metastatic potential due to repression of epithelial-mesenchymal transition (EMT). Overexpression of
LCN2
in CCA cells increased cell metastatic potential. We showed for the first time that the N-myc downstream regulated gene 1 (
NDRG1
) and
NDRG2
, known as tumor suppressor genes, are negatively regulated by LCN2 in CCA cells. LCN2 concentration in bile was higher in patients with CCA than that in patients with gallstones, with a cutoff value of 20.08 ng/ml making this a potential diagnostic marker. Higher
LCN2
expression was associated with worse survival in patients with CCA.
LCN2
is a promising target for CCA treatment and bile LCN2 level is a potential diagnostic marker for CCA. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/srep36138 |