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Article

Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients

  • Authors:
    • Baosong Xie
    • Guanying Zheng
    • Hongru Li
    • Xiujuan Yao
    • Rujun Hong
    • Ruihui Li
    • Wenxiang Yue
    • Yusheng Chen
  • View Affiliations / Copyright

    Affiliations: Department of Respiratory Medicine, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China
  • Pages: 2715-2723
    |
    Published online on: February 3, 2016
       https://doi.org/10.3892/mmr.2016.4852
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Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive interstitial fibrosis, and is associated with a fatal outcome. The critical pathological mechanisms underlying IPF are largely unknown; however, accumulating evidence has indicated similarities between IPF and cancer. Therefore, the present study examined the expression levels of the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in Chinese patients with IPF, using an enzyme‑linked immunosorbent assay. To determine the effects of PTEN on the development of pulmonary fibrosis, PTEN was overexpressed in transforming growth factor (TGF)‑β1‑treated human embryonic lung fibroblasts (HFL‑I cells). The serum levels of PTEN were significantly lower in 42 patients with IPF, as compared with in the healthy controls. In addition, PTEN overexpression enhanced apoptosis, and suppressed basal levels of proliferation and migration in fibroblasts. Notably, PTEN was able to specifically inhibit TGF‑β1‑induced proliferation and migration of the cells. Overexpression of PTEN also suppressed phosphorylation of Akt and Smad3, and decreased the expression levels of numerous proteins with critical roles in TGF‑β1‑induced fibrosis, including α‑smooth muscle actin, matrix metalloproteinase (MMP)‑2 and MMP‑9. These results indicated that PTEN may inhibit TGF‑β1‑mediated myofibroblast differentiation of fibroblasts by attenuating signaling via the phosphatidylinositol 3‑kinase/Akt and TGF‑β/Smad3 pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Xie B, Zheng G, Li H, Yao X, Hong R, Li R, Yue W and Chen Y: Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients. Mol Med Rep 13: 2715-2723, 2016.
APA
Xie, B., Zheng, G., Li, H., Yao, X., Hong, R., Li, R. ... Chen, Y. (2016). Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients. Molecular Medicine Reports, 13, 2715-2723. https://doi.org/10.3892/mmr.2016.4852
MLA
Xie, B., Zheng, G., Li, H., Yao, X., Hong, R., Li, R., Yue, W., Chen, Y."Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients". Molecular Medicine Reports 13.3 (2016): 2715-2723.
Chicago
Xie, B., Zheng, G., Li, H., Yao, X., Hong, R., Li, R., Yue, W., Chen, Y."Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients". Molecular Medicine Reports 13, no. 3 (2016): 2715-2723. https://doi.org/10.3892/mmr.2016.4852
Copy and paste a formatted citation
x
Spandidos Publications style
Xie B, Zheng G, Li H, Yao X, Hong R, Li R, Yue W and Chen Y: Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients. Mol Med Rep 13: 2715-2723, 2016.
APA
Xie, B., Zheng, G., Li, H., Yao, X., Hong, R., Li, R. ... Chen, Y. (2016). Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients. Molecular Medicine Reports, 13, 2715-2723. https://doi.org/10.3892/mmr.2016.4852
MLA
Xie, B., Zheng, G., Li, H., Yao, X., Hong, R., Li, R., Yue, W., Chen, Y."Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients". Molecular Medicine Reports 13.3 (2016): 2715-2723.
Chicago
Xie, B., Zheng, G., Li, H., Yao, X., Hong, R., Li, R., Yue, W., Chen, Y."Effects of the tumor suppressor PTEN on the pathogenesis of idiopathic pulmonary fibrosis in Chinese patients". Molecular Medicine Reports 13, no. 3 (2016): 2715-2723. https://doi.org/10.3892/mmr.2016.4852
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