Transforming growth factor-β transiently induces vimentin expression and invasive capacity in a canine mammary gland tumor cell line

被引：15

作者：

Yoshida, K. ^{[1
]}

Saito, T. ^{[1
]}

Kamida, A. ^{[1
]}

Matsumoto, K. ^{[1
]}

Saeki, K. ^{[1
]}

Mochizuki, M. ^{[1
]}

Sasaki, N. ^{[1
]}

Nakagawa, T. ^{[1
]}

机构：

[1] Univ Tokyo, Lab Vet Surg, Grad Sch Agr & Life Sci, Tokyo 1138657, Japan

来源：

RESEARCH IN VETERINARY SCIENCE | 2013年 / 94卷 / 03期

关键词：

Dog; Mammary gland tumor; EMT; TGF-beta; MET; xCELLigence RTCA; EPITHELIAL-MESENCHYMAL TRANSITIONS; TGF-BETA; IN-VITRO; PROGRESSION; NEOPLASMS; CANCER;

D O I：

10.1016/j.rvsc.2012.10.016

中图分类号：

S85 [动物医学（兽医学）];

学科分类号：

0906 ;

摘要：

The epithelial-mesenchymal transition (EMT) is a crucial event that occurs during cancer metastasis and can be induced by transforming growth factor-beta (TGF-beta) in various tumor cells in vitro. However, little is known about the effects of TGF-beta in canine mammary gland tumors (CMGTs). Here, we investigated the role of TGF-beta in CMGT. We observed that treatment of the CMGT cell line CHMp13a with TGF-beta 1 leads to transient induction of the mesenchymal marker vimentin. Real-time measurements of cellular electrical impedance also showed that CMGT invasiveness is transiently increased by TGF-beta 1 treatment, but is reversed after prolonged stimulation. This phenomenon is similar to the mesenchymal-epithelial transition (MET, the reverse phenomenon of EMT), and a process that is implicated in the establishment of secondary metastatic lesions. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：539 / 541

页数：3

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