Transforming growth factor β1 promotes migration and invasion in HepG2 cells: Epithelial‑to‑mesenchymal transition via JAK/STAT3 signaling
Autor: | Xiaolong Lin, Xiao-Juan Fan, Xue-Mei Hu, Wei-Wen Zou, Yongquan� Pan, Yuanbo Liu, Huijun Hu, Mi-Hua Liu |
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Rok vydání: | 2017 |
Předmět: |
STAT3 Transcription Factor
0301 basic medicine Epithelial-Mesenchymal Transition medicine.medical_treatment Transforming Growth Factor beta1 03 medical and health sciences Twist transcription factor 0302 clinical medicine Cell Movement Genetics medicine Humans Neoplasm Invasiveness Epithelial–mesenchymal transition Neoplasm Metastasis RNA Small Interfering STAT3 Cell Proliferation Janus Kinases transforming growth factor β1 biology Liver Neoplasms Twist-Related Protein 1 Articles Hep G2 Cells General Medicine Tyrphostins Cell biology Gene Expression Regulation Neoplastic 030104 developmental biology Cytokine 030220 oncology & carcinogenesis signal transducer and activator of transcription 3 biology.protein Cancer research STAT protein epithelial-to-mesenchymal transition Signal transduction Janus kinase Signal Transduction Transforming growth factor |
Zdroj: | International Journal of Molecular Medicine |
ISSN: | 1791-244X 1107-3756 |
Popis: | 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. |
Databáze: | OpenAIRE |
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