Literature DB >> 22884073

The effects of genistein on transforming growth factor-β1-induced invasion and metastasis in human pancreatic cancer cell line Panc-1 in vitro.

Lei Han1, Hong-Wei Zhang, Wen-Ping Zhou, Guang-Ming Chen, Ke-Jian Guo.   

Abstract

BACKGROUND: Pancreatic cancer is a devastating disease with the worst mortality rate. Therefore, a rational strategy for future drug development is critical. Genistein is a small, biologically active flavonoid that is found in high amounts in soy. This important compound supports a wide variety of biological activities, but is best known for its ability to inhibit cancer progression.
METHODS: Transwell chamber assay was performed to determine the effect of genistein on the invasion of the human pancreatic cancer cell line Panc-1 induced by transforming growth factor-β1 (TGF-b1) in the different condition (5 ng/ml 24 hours and 10 ng/ml 48 hours); Reverse transcription-polymerase chain reaction (RT-PCR) was used to estimate the mRNA levels of urinary plasminogen activator (uPA), matrix metallopeptidase 2/9 (MMP-2/9), Smad4, E-Cadherin and Vimentin; Western blotting was used to detect the protein levels of uPA, E-Cadherin, ERK1/2, P38 and P-P38, and the activity of MMP-2/9 protein were detected by gelatin zymography assay method. Cells structure was observed and analyzed by microscopy.
RESULTS: Genistein can inhibit effectively TGF-b1-induced invasion and metastasis in Panc-1 by Transwell assay, which is through regulating the mRNA and protein expression of uPA and MMP2, but not MMP9 by RT-PCR/Western blotting, and is positively correlated with the concentration of genistein. At the same time, genistein also could improve the progress of epithelial-mesenchymal transition (EMT) via morphology observation using light microscopy/transmission electron microscopy (TEM), which is mediated by the down-regulation of E-cadherin and the up-regulation of vimentin.
CONCLUSIONS: TGF-b1 mediates EMT process via numerous intracellular signal transduction pathways. The potential molecular mechanisms are all or partly through Smad4-dependent and -independent pathways (p38 MAPK) to regulate the antitumor effect of genistein.

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Year:  2012        PMID: 22884073

Source DB:  PubMed          Journal:  Chin Med J (Engl)        ISSN: 0366-6999            Impact factor:   2.628


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