FSTL1 suppresses tumor cell proliferation, invasion and survival in non-small cell lung cancer

Ni,Xiaolei; Cao,Xiaoming; Wu,Yongquan; Wu,Jian

doi:10.3892/or.2017.6061

FSTL1 suppresses tumor cell proliferation, invasion and survival in non-small cell lung cancer

Authors:
- Xiaolei Ni
- Xiaoming Cao
- Yongquan Wu
- Jian Wu
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Affiliations: Department of Medical Oncology, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China, Department of Respiratory Medicine, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China, Department of Cardiothoracic Surgery, The First Hospital of Longyan Affiliated to Fujian Medical University, Longyan, Fujian, P.R. China
Published online on: October 31, 2017 https://doi.org/10.3892/or.2017.6061
Pages: 13-20
Copyright: © Ni et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Follistatin like-1 (FSTL1) is a secreted glycoprotein involved in a series of physiological and pathological processes. However, its contribution to the development of cancer, especially the pathogenesis of NSCLC, remains to be elucidated. We explored the expression, function, and molecular mechanism of FSTL1 in NSCLC. In this study, we detected the expression of FSTL1 in a panel of NSCLC cell lines and lung normal epithelial cell line by qRT-PCR and western blot analysis and found that FSTL1 was downregulated in NSCLC cells compared with normal control. Knockdown of FSTL1 with different shRNA sequences result in increased cell proliferation and cell migration, invasion and reduced cell apoptosis in A549 cell line with high FSTL1 endogenous level. FSTL1 overexpression in H446 cell line with low FSTL1 endogenous level suppressed cell proliferation and migration, invasion and increased cell apoptosis. Knockdown and overexpression of FSTL1 caused altered cell cycle. Reduced cell apoptosis was revealed in FSTL1 knockdown cells accompanied by increased FAS expression and decreased FASL, cleaved caspase‑3 and ‑7 expression. By contrast, overexpression of FSTL1 caused reduced FAS level and increased activated caspase‑3 and ‑7 expression, which may lead to increased cell apoptosis. Moreover, the changed migration and invasion ability in FSTL1 sufficient or deficient cells may be caused by alterations in MMP2, MMP3 and MMP9 expression. Altogether, our results revealed the critical tumor-suppression function of FSTL1 in NSCLC progression, suggesting that FSTL1 might be an important factor in NSCLC progression.

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