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
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