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Formation of Human Prostate Epithelium Using Tissue Recombination of Rodent Urogenital Sinus Mesenchyme and Human Stem Cells

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Published on: June 22, 2013

[Epithelial-mesenchymal transition and human fetal prostate development].

Jian-cheng Zhou¹, Guo-dong Zhu, Kai-jie Wu

¹Department of Urology, The First Affiliated Hospital ofXi'an Jiaotong University, Xi'an, Shaanxi 710061, China. zhoujc1207@yahoo.com.cn

Zhonghua Nan Ke Xue = National Journal of Andrology

|March 17, 2011

Summary

Epithelial-mesenchymal transition (EMT) and Twist1 are crucial for human fetal prostate development, influencing early tubule formation and later epithelial differentiation.

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Area of Science:

Urology
Developmental Biology
Cell Biology

Background:

The development of the human fetal prostate involves complex cellular processes.
Epithelial-mesenchymal transition (EMT) is a known mechanism in embryonic development.
Twist1 is a key transcriptional regulator implicated in EMT.

Purpose of the Study:

To investigate the role and significance of EMT and its regulator Twist1 in human fetal prostate development.
To analyze the expression patterns of EMT markers and Twist1 during prostate organogenesis.

Main Methods:

Analysis of 25 human fetal prostate specimens (16-39 weeks gestation).
Immunohistochemistry was used to detect E-Cadherin, N-Cadherin, Vimentin, and Twist1.
Expression patterns were correlated with developmental stages.

Main Results:

E-Cadherin was localized to the fetal prostate epithelium.
Vimentin, N-Cadherin, and Twist1 were found in both epithelium and stroma.
E-Cadherin expression increased with gestation, while Vimentin, N-Cadherin, and Twist1 decreased.

Conclusions:

EMT plays a role in human fetal prostate development.
EMT may facilitate epithelial cell motility for tubule formation in early gestation.
EMT may also support prostate epithelial differentiation in later stages.