Gene expression patterns in human embryonic stem cells and human pluripotent germ cell tumors

TLDR

Little is known about the transcriptional profiles of human embryonic stem cells and the mechanisms underlying their pluripotency. The study aims to identify commonalities among transcriptional profiles of human pluripotent cells and to uncover clues to the genesis of human germ cell tumors. The authors compared expression profiles of human ES cell lines, germ cell tumor cell lines and samples, somatic cell lines, and testicular tissue using cDNA microarray analysis. Hierarchical clustering showed that the five human ES cell lines clustered tightly together, sharing many similarities with embryonal carcinoma cells and, to a lesser extent, with seminoma samples, and 895 genes were identified as significantly overexpressed in ES and embryonal carcinoma lines, suggesting roles in maintaining pluripotency.

Abstract

Remarkably little is known about the transcriptional profiles of human embryonic stem (ES) cells or the molecular mechanisms that underlie their pluripotency. To identify commonalties among the transcriptional profiles of different human pluripotent cells and to search for clues into the genesis of human germ cell tumors, we compared the expression profiles of human ES cell lines, human germ cell tumor cell lines and tumor samples, somatic cell lines, and testicular tissue samples by using cDNA microarray analysis. Hierarchical cluster analysis of gene expression profiles showed that the five independent human ES cell lines clustered tightly together, reflecting highly similar expression profiles. The gene expression patterns of human ES cell lines showed many similarities with the human embryonal carcinoma cell samples and more distantly with the seminoma samples. We identified 895 genes that were expressed at significantly greater levels in human ES and embryonal carcinoma cell lines than in control samples. These genes are candidates for involvement in the maintenance of a pluripotent, undifferentiated phenotype.