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Title 

Modulation of E-cadherin expression by K-Ras: involvement of DNA methyltransferase-3b

Authors 

O Song KwonSook-Jung JeongSunOk KimL HeHee Gu LeeK L JangH OsadaM JungBo Yeon KimJong Seog Ahn

Publisher 

Oxford University Press (OUP)

Issue Date 

2010

Citation 

Carcinogenesis, vol. 31, no. 7, pp. 1194-1201

Abstract 

E-cadherin, as a tumor suppressor, plays an important role for intercellular adhesion involved in metastasis. Although K-Ras is highly expressed in a variety of cancers, the regulation of E-cadherin expression by K-Ras in association with DNA methylation and cell metastasis has not been completely clarified. In this study, E-cadherin expression was repressed in 267B1/K-Ras human epithelial prostate cancer cells stably overexpressing K-Ras, resulting from hypermethylation of E-cadherin promoter as evidenced by methylation-specific polymerase chain reaction (PCR), bisulfite sequencing, real-time reverse transcription-PCR and western blot analysis. The increased level of DNA methyltransferase (DNMT) 3b in 267B1/K-Ras cells was reduced by small interfering RNA-mediated knockdown of k-ras, whereas DNMT1 and DNMT3a did not change regardless of K-Ras or 5-aza-2′-deoxycytidine (5′-AzaC) treatment. Furthermore, binding of DNMT3b to E-cadherin promoter was increased in 267B1/K-Ras cells but was reduced by 5′-AzaC, as revealed by chromatin immunoprecipitation assay, which was in agreement with cell aggregation and invasive mobilization of the cells. Hence, our data suggest that increased binding of DNMT3b to E-cadherin promoter region by K-Ras cause promoter hypermethylation for reduced expression of E-cadherin, leading to the decreased cell aggregation and increased metastasis of human prostate cancer cells overexpressing K-Ras.

ISSN 

0143-3334

Link 

http://dx.doi.org/10.1093/carcin/bgq071

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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