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Open Access Research article

Stromal fibroblasts in the microenvironment of gastric carcinomas promote tumor metastasis via upregulating TAGLN expression

Beiqin Yu1, Xuehua Chen1, Jianfang Li1, Ying Qu1, Liping Su1, Yibing Peng2, Jian Huang3, Jun Yan4, Yingyan Yu1, Qinlong Gu1, Zhenggang Zhu1 and Bingya Liu1*

Author Affiliations

1 Key Laboratory of Shanghai Gastric Neoplasms, Department of Surgery, Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

2 Department of Laboratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China

3 National Human Genome Center at Shanghai, Shanghai 201203, China

4 James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202, USA

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BMC Cell Biology 2013, 14:17  doi:10.1186/1471-2121-14-17

Published: 19 March 2013

Abstract

Background

Fibroblasts play a critical role in tumorigenesis, tumor progression and metastasis. However, their detailed molecular characteristics and clinical significance are still elusive. TAGLN is an actin-binding protein that plays an important role in tumorigenesis.

Results

We investigated the interaction between cancer cells and the tumor microenvironment to determine how the fibroblasts from human gastric carcinoma facilitate tumorigenesis through TAGLN. QRT-PCR and Western blot indicated that TAGLN expression was upregulated in gastric carcinoma-associated fibroblasts (CAFs) that promote gastric cancer cell migration and invasion. Using small interfering RNA (siRNA), we found that CAFs enhanced tumor metastasis through upregulated TAGLN in vitro and in vivo. The expression of matrix metalloproteinase-2 (MMP-2) was significantly lower after TAGLN knock-down by siRNA. TAGLN levels were elevated in human gastric cancer stroma than normal gastric stroma and associated with differentiation and lymph node metastasis of gastric cancer.

Conclusion

CAFs may promote gastric cancer cell migration and invasion via upregulating TAGLN and TAGLN induced MMP-2 production.

Keywords:
TAGLN; Fibroblast; Microenvironment; Tumor metastasis; Gastric carcinoma