Please use this identifier to cite or link to this item: https://doi.org/10.1002/ijc.2910590512
Title: A HLA class I cis-regulatory element whose activity can be modulated by hormones
Authors: Sim, B.C. 
Hui, K.M. 
Issue Date: 1994
Citation: Sim, B.C., Hui, K.M. (1994). A HLA class I cis-regulatory element whose activity can be modulated by hormones. International Journal of Cancer 59 (5) : 646-654. ScholarBank@NUS Repository. https://doi.org/10.1002/ijc.2910590512
Abstract: To elucidate the basis of the down-regulation in major histocompatibility complex (MHC) class I gene expression and to identify possible DNA-binding regulatory elements that have the potential to interact with class I MHC genes, we have studied the transcriptional regulation of class I HLA genes in human breast carcinoma cells. A 9 base pair (bp) negative cis-regulatory element (NRE) has been identified using band-shift assays employing DNA sequences derived from the 5'-flanking region of HLA class I genes. This 9-bp element, GTCATGGCG, located within exon 1 of the HLA class I gene, can potently inhibit the expression of a heterologous thymidine kinase (TK) gene promoter and the HLA enhancer element. Furthermore, this regulatory element can exert its suppressive function in either the sense or anti-sense orientation. More interestingly, NRE can suppress dexamethasone-mediated gene activation in the context of the reported glucocorticoid responsive element (GRE) in MCF-7 cells but has no influence on the estrogen-mediated transcriptional activation of MCF-7 cells in the context of the reported estrogen-responsive element (ERE). Furthermore, the presence of such a regulatory element within the HLA class I gene whose activity can be modulated by hormones correlates well with our observation that the level of HLA class I gene expression can be down-regulated by hormones in human breast carcinoma cells. Such interactions between negative regulatory elements and specific hormone trans-activators are novel and suggest a versatile form of transcriptional control.
Source Title: International Journal of Cancer
URI: http://scholarbank.nus.edu.sg/handle/10635/111756
ISSN: 00207136
DOI: 10.1002/ijc.2910590512
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