Methylation of the E-Cadherin Gene Promoter Correlates With Progression of Prostate Cancer

Li, Long-Cheng; Zhao, Hong; Nakajima, Koichi; Oh, Bong Ryoul; Ribeiro-Filho, Leopoldo; Carroll, Peter R.; Dahiya, Rajvir

doi:10.1016/s0022-5347(05)66047-8

Cited by 109 publications

(63 citation statements)

References 23 publications

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“…The transformation of normal mammary epithelial cells into carcinoma and the subsequent progression to invasion and metastasis involve the accumulation of numerous genetic 'hits,' including the activation or ampliWcation of dominant oncogenes and the deletion or inactivating mutation of key tumor suppressor genes. It has known that tumor suppressor genes may also be transcriptionally silenced in association with aberrant promoter-region CpG island methylation (Li et al 2001;Nass et al 2000). Recently, promoter hypermethylation has been identiWed and associated with loss of expression of many potentially interesting genes in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Protein expression and gene promoter hypermethylation of CD99 in transitional cell carcinoma of urinary bladder

Xuan

Kim

Lin

2010

J Cancer Res Clin Oncol

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Section: Discussionmentioning

confidence: 99%

Protein expression and gene promoter hypermethylation of CD99 in transitional cell carcinoma of urinary bladder

Xuan

Kim

Lin

2010

J Cancer Res Clin Oncol

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“…Other mechanisms such as transacting pathways [14] and chromatin rearrangement [15] have also been observed, but only limited in several cancers. In contrast, alterations in DNA methylation patterns have recently been reported to be commonly found in cancers, such as oral [16,17], hepatocellular [18,19], breast [20,21], and prostate [21,22] cancers.…”

Section: Introductionmentioning

confidence: 99%

Clinical Evaluation of E-cadherin Expression and its Regulation Mechanism in Epithelial Ovarian Cancer

Xin

2006

Clin Exp Metastasis

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E-cadherin plays an important role in maintaining tissue architecture. Loss of E-cadherin expression has often been associated with cancer metastasis. This study assessed the immuno-expression of E-cadherin and methylation of CDH1 and correlated them with clinical features in primary epithelial ovarian cancer. Moreover, epithelial ovarian cancer cell SKOV3 was used to explore the mechanism how the demethylating agent 5-Aza inhibited cancer metastasis. Of 80 patients with primary ovarian cancer, we found that decreased immunoexpression pattern of E-cadherin was associated with clinical stage, lymph node metastasis, and degree of differentiation. Methylation of CDH1 detected by MSP occurred frequently and was correlated with reduced expression of E-cadherin protein. 5-Aza treatment could lead to re-expression of functional E-cadherin, followed by decreased MMP-2 and MMP-9 activity and inhibition of cell invasion in SKOV3 cells. Therefore, we conclude that assessment of E-cadherin immunoreactivity or methylation of CDH1 may be a useful prognostic indicator in ovarian cancer, complementary to established prognostic factors. The mechanism underlying 5-Aza's anti-metastasis activity is associated with restored functional expression of E-cadherin and decreased MMPs activity. Correction of aberrant DNA methylation by 5-Aza may provide a new strategy for ovarian cancer prevention and therapy.

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“…Epigenetic inactivation of tumor suppressor genes through DNA methylation in CpGrich promoter regions contributes to tumorigenesis (Baylin and Herman, 2000;Jones and Baylin, 2002). In prostate cancer, aberrant methylation is involved in the inactivation of various important genes such as E-cadherin, CD44, RASSF1A, GSTP1, the endothelin B receptor, p16, the androgen receptor gene, the retinoic acid receptor beta (RARbeta), the estrogen receptor beta (ER-beta) and the caveolin-1 gene (Lee et al, 1994;Nelson et al, 1997;Cui et al, 2001;Kito et al, 2001;Li et al, 2000Li et al, , 2001Nakayama et al, 2001;Pao et al, 2001;Kuzmin et al, 2002;Liu et al, 2002). When tested, loss of the expression of these genes was associated with CpG island hypermethylation, and expression could be restored after treatment with 5-aza-2 0 -deoxycytidine (5-Aza-CdR), a DNA methyltransferase inhibitor.…”

Section: Introductionmentioning

confidence: 99%

Methylation of the retinoid response gene TIG1 in prostate cancer correlates with methylation of the retinoic acid receptor beta gene

2003

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Methylation of CpG islands and associated gene silencing may lead to malignant progression, but the mechanisms of CpG island methylation in cancer are unknown. The tazarotene-induced gene 1 (TIG1), also known as retinoid acid (RA) receptor-responsive 1 gene was first identified as an RA-responsive gene and was shown to be downregulated in prostate cancer. Here, we show that this downregulation is caused by the methylation of the promoter and CpG island of TIG1. TIG1 was methylated in 26 of 50 (52%) primary prostate cancers, but was not methylated in normal tissues or benign hyperplasias. Three of four tumors that metastasized, five of six that were poorly differentiated and all that were assigned a Gleason score higher than 8 (7/7) were methylated in the promoter of TIG1. The samples with peripheral invasion were more frequently methylated (21/32, 66%) than tissues without peripheral invasion (5/18, 28%). In addition, Gleason 7-10 cancers (21/30, 70%) were significantly more frequently methylated compared with Gleason 4-6 cancers (4/18, 22%) (Po0.01). The retinoic acid receptor beta (RAR-beta) gene was frequently methylated as well (42/50, 84%). When TIG1 showed methylation, RAR-beta was also methylated (25/26 samples). In almost all samples where RAR-beta was not methylated, TIG1 was also in an unmethylated state (14/15 samples). The methylation of TIG1 and RAR-beta was positively correlated (r ¼ 0.35; P ¼ 0.017). It is possible that the methylation of the retinoid response gene TIG1 occurred in response to the methylation and inactivation of RAR-beta. These observations may contribute to our understanding of mechanistic events leading to CpG island methylation in cancer.

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Methylation of the E-Cadherin Gene Promoter Correlates With Progression of Prostate Cancer

Cited by 109 publications

References 23 publications

Protein expression and gene promoter hypermethylation of CD99 in transitional cell carcinoma of urinary bladder

Protein expression and gene promoter hypermethylation of CD99 in transitional cell carcinoma of urinary bladder

Clinical Evaluation of E-cadherin Expression and its Regulation Mechanism in Epithelial Ovarian Cancer

Methylation of the retinoid response gene TIG1 in prostate cancer correlates with methylation of the retinoic acid receptor beta gene

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