Unmethylated E‐Cadherin gene expression is significantly associated with metastatic human prostate cancer cells in bone

Saha, Bodhisattwa; Kaur, Pavinder; Tsao‐Wei, Denice; Naritoku, Wesley Y.; Groshen, Susan; Datar, Ram H.; Jones, L. W.; Imam, S. Ashraf

doi:10.1002/pros.20836

Cited by 24 publications

(24 citation statements)

References 30 publications

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“…On the other hand some recent articles objected to this issue. Saha et al (27) reported that loss of e-cadherin gene expression is caused by reversible epigenetic mechanisms, and showed that e-cadherin gene expression was present in metastatic bone lesions of prostate carcinoma. it was hypothesized that e-cadherin gene expression might be the last fact to provide advantage tumor cells to make clusters in metastatic areas (26).…”

Section: Resultsmentioning

confidence: 99%

Expression of E-Cadherin, Cox-2, P53 and BCL-2 in Prostate Carcinomas: Correlation with Tumor Differentiation and Metastatic Potential

Özekinci

Uzunlar

Şentürk

et al. 2010

Biotechnology & Biotechnological Equipment

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Section: Resultsmentioning

confidence: 99%

Expression of E-Cadherin, Cox-2, P53 and BCL-2 in Prostate Carcinomas: Correlation with Tumor Differentiation and Metastatic Potential

Özekinci

Uzunlar

Şentürk

et al. 2010

Biotechnology & Biotechnological Equipment

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“…Likewise, enhancer of zeste homolog 2 (EZH2), which is involved in gene silencing by histone methylation, is overexpressed in advanced PC and can mediate the silencing of E-cadherin [166]. Interestingly, a survey of primary PC samples and metastatic bone biopsies showed that 70 % of primary PC samples have a methylated E-cadherin promoter with heterogeneous E-cadherin expression, while 87 % of metastatic bone biopsies contain an unmethylated E-cadherin promoter with homogenous E-cadherin expression [167]. Together, these results demonstrate that EMT can be epigenetically regulated and provide a mechanism linking EMT with PC progression.…”

Section: Preclinical Evidence Of Ep In Pcmentioning

confidence: 99%

The role of epithelial plasticity in prostate cancer dissemination and treatment resistance

Bitting

Schaeffer

Somarelli

et al. 2014

Cancer Metastasis Rev

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Nearly 30,000 men die annually in the USA of prostate cancer, nearly uniformly from metastatic dissemination. Despite recent advances in hormonal, immunologic, bone-targeted, and cytotoxic chemotherapies, treatment resistance and further dissemination are inevitable in men with metastatic disease. Emerging data suggests that the phenomenon of epithelial plasticity, encompassing both reversible mesenchymal transitions and acquisition of stemness traits, may underlie this lethal biology of dissemination and treatment resistance. Understanding the molecular underpinnings of this cellular plasticity from preclinical models of prostate cancer and from biomarker studies of human metastatic prostate cancer has provided clues to novel therapeutic approaches that may delay or prevent metastatic disease and lethality over time. This review will discuss the preclinical and clinical evidence for epithelial plasticity in this rapidly changing field and relate this to clinical phenotype and resistance in prostate cancer while suggesting novel therapeutic approaches.

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“…Chromatin immunoprecipitation (CHIP) analysis showed that MMSET binds directly to TWIST1 locus, suggesting a direct role of MMSET in the regulation of TWIST1 expression [84]. The classical epithelial marker E-cadherin is often found to be silenced in PCa due to promoter methylation [85–86]. It is intriguing to note that methylation of E-cadherin is a priming event that helps in creating a permissive environment for outgrowth and continued morphogenesis of prostatic ducts at different stages of the development [87].…”

Section: Extracellular Signals To Regulate Emtmentioning

confidence: 99%

Role of Epithelial Mesenchymal Transition in Prostate Tumorigenesis

Khan¹,

Hamid²,

Adhami³

et al. 2015

CPD

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Globally, the cancer associated deaths are generally attributed to the spread of cancerous cells or their features to the nearby or distant secondary organs by a process known as metastasis. Among other factors, the metastatic dissemination of cancer cells is attributed to the reactivation of an evolutionary conserved developmental program known as epithelial to mesenchymal transition (EMT). During EMT, fully differentiated epithelial cells undergo a series of dramatic changes in their morphology, along with loss of cell to cell contact and matrix remodeling into less differentiated and invasive mesenchymal cells. Many studies provide evidence for the existence of EMT like states in prostate cancer (PCa) and suggest its possible involvement in PCa progression and metastasis. At the same time, the lack of conclusive evidence regarding the presence of full EMT in human PCa samples has somewhat dampened the interest in the field. However, ongoing EMT research provides new perspectives and unveils the enormous potential of this field in tailoring new therapeutic regimens for PCa management. This review summarizes the role of many transcription factors and other molecules that drive EMT during prostate tumorigenesis.

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Unmethylated E‐Cadherin gene expression is significantly associated with metastatic human prostate cancer cells in bone

Cited by 24 publications

References 30 publications

Expression of E-Cadherin, Cox-2, P53 and BCL-2 in Prostate Carcinomas: Correlation with Tumor Differentiation and Metastatic Potential

Expression of E-Cadherin, Cox-2, P53 and BCL-2 in Prostate Carcinomas: Correlation with Tumor Differentiation and Metastatic Potential

The role of epithelial plasticity in prostate cancer dissemination and treatment resistance

Role of Epithelial Mesenchymal Transition in Prostate Tumorigenesis

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