Research Summary: Comparison of Gene Expression Profiles in Chromate Transformed BEAS-2B Cells



Hexavalent chromium [Cr(VI)] is a potent human carcinogen.
Occupational exposure has been associated with increased risk of respiratory
cancer. Multiple mechanisms have been shown to contribute to Cr(VI) induced
carcinogenesis, including DNA damage, genomic instability, and epigenetic
modulation, however, the molecular mechanism and downstream genes mediating
chromium’s carcinogenicity remain to be elucidated.


We established chromate transformed cell lines by chronic exposure of normal
human bronchial epithelial BEAS-2B cells to low doses of Cr(VI) followed by
anchorage-independent growth. These transformed cell lines not only
exhibited consistent morphological changes but also acquired altered and
distinct gene expression patterns compared with normal BEAS-2B cells and
control cell lines (untreated) that arose spontaneously in soft agar.
Interestingly, the gene expression profiles of six Cr(VI) transformed cell
lines were remarkably similar to each other yet differed significantly from
that of either control cell lines or normal BEAS-2B cells. A total of 409
differentially expressed genes were identified in Cr(VI) transformed cells
compared to control cells. Genes related to cell-to-cell junction were
upregulated in all Cr(VI) transformed cells, while genes associated with the
interaction between cells and their extracellular matrices were
down-regulated. Additionally, expression of genes involved in cell
proliferation and apoptosis were also changed.


This study is the first to report gene expression profiling of Cr(VI)
transformed cells. The gene expression changes across individual chromate
exposed clones were remarkably similar to each other but differed
significantly from the gene expression found in anchorage-independent clones
that arose spontaneously. Our analysis identified many novel gene expression
changes that may contribute to chromate induced cell transformation, and
collectively this type of information will provide a better understanding of
the mechanism underlying chromate carcinogenicity.


Publisher: Public Library of Science

Date Published: 18-March-2011

Author(s): Sun H., Clancy H., Kluz T., Zavadil J., Costa M.


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