Literature DB >> 24011634

Interaction between non-small-cell lung cancer cells and fibroblasts via enhancement of TGF-β signaling by IL-6.

Abulimiti Abulaiti1, Yasushi Shintani, Soichiro Funaki, Tomoyuki Nakagiri, Masayohi Inoue, Noriyoshi Sawabata, Masato Minami, Meinoshin Okumura.   

Abstract

INTRODUCTION: Fibroblasts are key components of the tumor microenvironment. We clarified the role of transforming growth factor (TGF)-β and interleukin (IL)-6 in the interaction between fibroblasts and non-small-cell lung cancer (NSCLC) cells.
METHODS: We used NSCLC cells (A549, NCI-H358) and normal human lung fibroblast (NHLF) cells to evaluate phenotypic changes in the presence of human IL-6, TGF-β1, and conditioned media (CM) from these cells. Possible pathways were evaluated with SB431542, a TGF-β receptor inhibitor, or an anti-human IL-6 receptor neutralizing antibody (IL-6R-Ab).
RESULTS: A549 and NCI-H358 cells incubated with IL-6 (50 ng/mL) and TGF-β1 (2 ng/mL) showed significantly increased epithelial-mesenchymal transition (EMT) signaling compared to those treated with TGF-β1 alone. Furthermore, NHLF cells were synergistically activated by IL-6 and TGF-β1. IL-6 increased the expression of TGF-β type I receptors on the surface of A549, NCI-H358 and NHLF cells and enhanced TGF-β signaling. TGF-β1 induced phenotypic changes were attenuated by IL-6R-Ab. NHLF cells were activated and A549 cells showed induction of EMT in response to CM from the other cell type. These activities were attenuated by SB431542 or IL-6R-Ab, suggesting that interplay between NSCLC cells and NHLF may lead to increased EMT signaling in NSCLC cells and activation of NHLF cells through TGF-β and IL-6 signaling. Subcutaneous co-injection of A549 and NHLF cells into mice resulted in a high rate of tumor formation compared with injection of A549 cells without NHLF cells. SB431542 or IL-6R-Ab also attenuated the tumor formation enhanced by co-injection of the two cell types.
CONCLUSION: IL-6 enhanced epithelial cell EMT and stimulated tumor progression by enhancing TGF-β signaling. IL-6 and TGF-β may play a contributing role in maintenance of the paracrine loop between these two cytokines in the communication between fibroblasts and NSCLC cells for tumor progression.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Entities:  

Keywords:  Epithelial–mesenchymal transition; Fibroblasts; IL-6; Non-small-cell lung cancer; TGF-β

Mesh:

Substances:

Year:  2013        PMID: 24011634     DOI: 10.1016/j.lungcan.2013.08.008

Source DB:  PubMed          Journal:  Lung Cancer        ISSN: 0169-5002            Impact factor:   5.705


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