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Chinese Journal of Stomatological Research(Electronic Edition) ›› 2012, Vol. 6 ›› Issue (01): 29-37. doi: 10.3877/cma.j.issn.1674-1366.2012.01.005

• Original Articles • Previous Articles    

Experiment study on the role and mechanism of TGF-β1/ERK1/2/MMP-2 signaling pathways in the migration and invasion process of ACC

Hong-liang XIE1, Bin ZHANG1,(), Zhi-ying XU1, Qi-Xiang LIANG1   

  1. 1.Department of Oral and Maxillofacial Surgery, Sun Yat-Sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510120, China
  • Received:2011-09-14 Online:2012-02-01 Published:2025-02-20
  • Contact: Bin ZHANG

Abstract:

Objective

To investigate the role of TGF-β1/ERK1/2/MMP-2 signaling pathways in the migration and invasion process of salivary adenoid cystic carcinoma cells.

Methods

ACC-2 cell line were used in this study. The proliferation of ACC-2 cell line was observed by MTT assay; cell migration and invasion ablity were examined by Transwell; the expression of MMP-2 in salivary adenoid cystic carcinoma cell lines was tested by Western blotting and Real-time PCR. The activity of ERK1/2 signaling pathway was measured by Western blotting. The effects of the ERK pathway specific inhibitors on TGF-β1-activated MMP-2 expression in ACC-2 cell lines were examined.

Results

TGF-β1 and U0126 could not enhance the proliferation of ACC-2 cells; TGF-β1 could enhance the migration and invasion abilities of them significantly. TGF-β1 enhanced expression of p-ERK1/2 and MMP-2 protein and MMP-2 mRNA in ACC-2 cells. When U0126 inhibited ERK1/2 pathway, the abilities of migration and invasion and production of MMP-2 stimulated by TGF-β1 were significantly inhibited in ACC-2 cells.

Conclusions

TGF-β1/ERK1/2/MMP-2 signaling pathways participate in the regulation of migration and invasion abilities in ACC. TGF-β1 can up-regulate ERK1/2, and then enhanced MMP-2 expression, promote the migration and invasion abilities of ACC. ERK1/2 may be turned to be a new target spot to prevent the invasion of ACC.

Key words: Adenoid cystic carcinoma, Transforming growth factor-β1, Extracellular regulated protein kinases, Matrix metalloproteinase-2, Signal path

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