Transforming growth factor β1 promotes migration and invasion in HepG2 cells: Epithelial‑to‑mesenchymal transition via JAK/STAT3 signaling

Transforming growth factor β1 (TGFβ1) is a cytokine with multiple functions. TGFβ1 significantly induces migration and invasion of liver cancer cells. However, the molecular mechanisms underlying this effect remain unclear. Epithelial‑to‑mesenchymal transition (EMT) is crucial for the development of...

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Published inInternational journal of molecular medicine Vol. 41; no. 1; pp. 129 - 136
Main Authors Lin, Xiao‑Long, Liu, Mihua, Liu, Yuanbo, Hu, Huijun, Pan, Yongquan�, Zou, Weiwen, Fan, Xiaojuan, Hu, Xuemei
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications UK Ltd 2018
D.A. Spandidos
Subjects
Binding sites
Biotechnology
Breast cancer
Gene expression
Growth factors
Kinases
Liver cancer
Lung cancer
Medical prognosis
Metastasis
Ovarian cancer
Proteins
Studies
Tumors
Beijing China
United States > US
China
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Summary:Transforming growth factor β1 (TGFβ1) is a cytokine with multiple functions. TGFβ1 significantly induces migration and invasion of liver cancer cells. However, the molecular mechanisms underlying this effect remain unclear. Epithelial‑to‑mesenchymal transition (EMT) is crucial for the development of invasion and metastasis in human cancers. The aim of the present study was to determine whether TGFβ1‑induced EMT promoted migration and invasion in HepG2 cells. The underlying mechanism and the effect of EMT on HepG2 cells were also investigated. The results demonstrated that TGFβ1 may induce EMT to promote migration and invasion of HepG2 cells, and this effect depends on activation of the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway. JAK/STAT3 signaling is involved in human malignancies, including lung cancer, and is implicated in cell transformation, tumorigenicity, EMT and metastasis. In the present study, TGFβ1 also activated JAK/STAT3 signaling in HepG2 cells and promoted Twist expression, but these events were abolished by treatment with the STAT3 inhibitor AG490. Additionally, Twist siRNA blocked TGFβ1‑induced EMT. Thus, TGFβ1 was shown to induce EMT, thereby promoting the migration and invasion of HepG2 cells via JAK/STAT3/Twist signaling.
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content type line 14
Contributed eually
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2017.3228