The Prognostic Impact of Leucine-Rich α-2-Glycoprotein-1 in Cholangiocarcinoma and Its Association With the IL-6/TGF-β1 Axis.


Journal

The Journal of surgical research
ISSN: 1095-8673
Titre abrégé: J Surg Res
Pays: United States
ID NLM: 0376340

Informations de publication

Date de publication:
08 2020
Historique:
received: 26 09 2019
revised: 28 01 2020
accepted: 09 03 2020
pubmed: 13 4 2020
medline: 10 9 2020
entrez: 13 4 2020
Statut: ppublish

Résumé

Leucine-rich α-2-glycoprotein-1 (LRG) has been found to participate in the development of various cancers through its involvement in TGF-β1-induced epithelial-mesenchymal transition (EMT) and/or angiogenesis and can be induced by inflammatory cytokines, such as IL-6. As we previously showed the implication of IL-6/TGF-β axis in EMT of cholangiocarcinoma cells, we herein explored the prognostic impact of LRG in postoperative intrahepatic cholangiocarcinoma (ICC) and assessed the association between tumor LRG and factors such as TGF-β1, IL-6, and the tumor microvessel density. We determined the expression of LRG, IL-6, TGF-β1, and CD31 in cancer tissues from 50 ICC patients by immunohistochemistry and analyzed their association with the prognosis. The LRG expression was closely associated with recurrence-free survival (RFS) and overall survival (OS) in postoperative ICC. A multivariate Cox regression model indicated that LRG as an independently associated with poor RFS (hazard ratio = 2.4339, P = 0.0354) and OS (hazard ratio = 2.8892, P = 0.0268). The LRG expression was significantly associated with the expression of TGF-β1 (P = 0.0003) and IL-6 (P = 0.0164). The upregulation of LRG in tumors was an independent prognostic factor in patients with postoperative ICC. LRG was closely associated with the TGF-β1 expression and seems to be an important member of the IL-6/TGF-β1 axis.

Sections du résumé

BACKGROUND
Leucine-rich α-2-glycoprotein-1 (LRG) has been found to participate in the development of various cancers through its involvement in TGF-β1-induced epithelial-mesenchymal transition (EMT) and/or angiogenesis and can be induced by inflammatory cytokines, such as IL-6. As we previously showed the implication of IL-6/TGF-β axis in EMT of cholangiocarcinoma cells, we herein explored the prognostic impact of LRG in postoperative intrahepatic cholangiocarcinoma (ICC) and assessed the association between tumor LRG and factors such as TGF-β1, IL-6, and the tumor microvessel density.
METHODS
We determined the expression of LRG, IL-6, TGF-β1, and CD31 in cancer tissues from 50 ICC patients by immunohistochemistry and analyzed their association with the prognosis.
RESULTS
The LRG expression was closely associated with recurrence-free survival (RFS) and overall survival (OS) in postoperative ICC. A multivariate Cox regression model indicated that LRG as an independently associated with poor RFS (hazard ratio = 2.4339, P = 0.0354) and OS (hazard ratio = 2.8892, P = 0.0268). The LRG expression was significantly associated with the expression of TGF-β1 (P = 0.0003) and IL-6 (P = 0.0164).
CONCLUSIONS
The upregulation of LRG in tumors was an independent prognostic factor in patients with postoperative ICC. LRG was closely associated with the TGF-β1 expression and seems to be an important member of the IL-6/TGF-β1 axis.

Identifiants

pubmed: 32278969
pii: S0022-4804(20)30138-4
doi: 10.1016/j.jss.2020.03.018
pii:
doi:

Substances chimiques

Glycoproteins 0
IL6 protein, human 0
Interleukin-6 0
LRG1 protein, human 0
TGFB1 protein, human 0
Transforming Growth Factor beta1 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

147-155

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Zhe Jin (Z)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Shogo Kobayashi (S)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Kunihito Gotoh (K)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Tsuyoshi Takahashi (T)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

Hidetoshi Eguchi (H)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan. Electronic address: heguchi@gesurg.med.osaka-u.ac.jp.

Testuji Naka (T)

Center for Intractable Immune Disease, Kochi University, Nangoku, Japan.

Masaki Mori (M)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan; Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Yuichiro Doki (Y)

Department of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Suita, Japan.

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