The glutathione S-transferase π gene (GSTπ) is highly expressed in estrogen receptor negative (ER-) but not expressed in ER+ human breast cancer cell lines. To define regulatory mechanisms of GSTπ gene expression, we analyzed both the activity of the GSTπ promoter and the posttranscriptional fate of GSTπ RNA sequences in three ER+ and three ER- breast cancer cell lines. Expression of a transiently transfected CAT reporter gene driven by the GSTπ promoter and 2203 nucleotides of 5'-flanking sequences were similar in all six cell lines regardless of ER status. Endogenous GSTπ transcription rates in nuclei isolated from ER- cells were quite low despite high steady state levels of cytoplasmic mRNA. Furthermore, the endogenous GSTπ gene was transcribed in ER+ nuclei at rates similar to those obtained in ER- nuclei. We determined the stabilities of mRNAs transcribed from the endogenous GSTπ gene (ER- cells) and from a stably transfected GSTπ cDNA expression vector (ER+ and ER- cells). The endogenous GSTπ mRNA was extraordinarily stable in ER- cells. Comparisons between transfected ER+ and ER- cells revealed no significant differences in the stabilities of transfection-derived GSTπ mRNA sequences. We conclude that GSTπ mRNA stability contributes significantly to the high levels of cytoplasmic mRNA observed in ER- cells, but that the differential expression of GSTπ in ER+ versus ER- cells is governed by other posttranscriptional processes.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Biological Chemistry|
|Publication status||Published - Jan 1 1992|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology