Literature DB >> 23053901

The down-regulation of Notch1 inhibits the invasion and migration of hepatocellular carcinoma cells by inactivating the cyclooxygenase-2/Snail/E-cadherin pathway in vitro.

Liang Zhou1, De-Sheng Wang, Qing-Jun Li, Wei Sun, Yong Zhang, Ke-Feng Dou.   

Abstract

BACKGROUND: The Notch signaling pathway plays an important role in cancer, but the mechanism by which Notch1 participates in invasion and migration of hepatocellular carcinoma (HCC) cells is unclear. AIMS: Our purpose is to confirm the anti-invasion and anti-migration effects of the down-regulation of Notch1 in HCC cells.
METHODS: The invasion and migration capacities of HCC cells were detected with Transwell cell culture chambers. The expressions of Notch1, Notch1 intracellular domain (N1ICD), E-cadherin, Snail, and cyclooxygenase-2 (COX-2) were analyzed by RT-PCR and/or western blotting. Notch1 and Snail were down-regulated by RNA interference, and COX-2 was inhibited by NS-398. Cell apoptosis was analyzed by MTT and flow cytometry.
RESULTS: In HCC cells, Snail, Notch1, and COX-2 were up-regulated, and E-cadherin was down-regulated in mRNA and/or protein levels. The down-regulation of Snail or Notch1 or the inhibition of COX-2, respectively, can increase the mRNA and protein expressions of E-cadherin and decrease the invasion and migration capabilities of HCC cell. Down-regulated Notch1 or inhibited COX-2 can reduce the mRNA and protein expressions of Snail. The down-regulation of Notch1 can also reduce the protein expression of COX-2. However, exogenous PGE2 can reverse the role of down-regulated Notch1. The results of MTT and flow cytometry showed that down-regulated Notch1 did not affect HCC cell viability.
CONCLUSIONS: Down-regulated Notch1 may be an effective approach to inactivating Snail/E-cadherin by regulating COX-2, which results in inhibiting the invasion and migration of HCC cells. The inhibitory effects of down-regulated Notch1 on cell invasion and migration were independent of apoptosis.

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Year:  2012        PMID: 23053901     DOI: 10.1007/s10620-012-2434-7

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  47 in total

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