Cited 3 times in

Clinicopathological significance of N-cadherin and VEGF in advanced gastric cancer brain metastasis and the effects of metformin in preclinical models.

Title
Clinicopathological significance of N-cadherin and VEGF in advanced gastric cancer brain metastasis and the effects of metformin in preclinical models.
Authors
Kyong-Hwa Jun;Jung Eun Lee;Seung-Ho Yang;Hyung-Min Chin;Young Il Kim;Hyun‑Joo Choi;Ji-Han Jung;Se Hoon Kim
Issue Date
2015
Journal Title
Oncology Reports
ISSN
1021-335X
Citation
Oncology Reports, Vol.34(4) : 2047~2053, 2015
Abstract
Gastric cancer is the second most common cause of cancer-related death worldwide. Although brain metastasis is a rare complication of gastric cancer, no standard therapy for gastric cancer brain metastasis has been established. We attempted to identify biological markers that predict brain metastasis, and investigated how to modulate such markers. A case-control study of patients newly diagnosed with gastric cancer who had developed brain metastasis during follow-up, was conducted. These patients were compared with patients who had advanced gastric cancer but no evidence of brain metastasis. Immunohistochemistry was used to analyze the expression of E-cadherin, N-cadherin, MSS1, claudin-3, claudin-4, Glut1, clusterin, ITGB4, vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR) and p53. The expression of VEGF tended to be higher in the case group (33.3 vs. 0%, p=0.055). Median survival was significantly correlated with vascular invasion (12 vs. 33 months, p=0.008) and N-cadherin expression (36 vs. 12 months, p=0.027). We also investigated the effects of metformin in tumor-bearing mouse models. VEGF expression was decreased and E-cadherin increased in the metformin‑treated group when compared with the control group. The expression of the mesenchymal marker MMP9 was decreased in the metformin-treated group. Brain metastasis of advanced gastric cancer was associated with the expression of VEGF. Metformin treatment may be useful for modulating the metastatic capacity by reducing VEGF expression and blocking epithelial-to-mesenchymal transition.
URI
http://www.spandidos-publications.com/or/34/4/2047

http://ir.ymlib.yonsei.ac.kr/handle/22282913/140951
DOI
10.3892/or.2015.4191.
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Pathology
Yonsei Authors
사서에게 알리기
  feedback
Files in This Item:
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse