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Watkins, Rachel J; Read, Martin L; Smith, Vicki E; Sharma, Neil; Reynolds, Gary M; Buckley, Laura; Doig, Craig; Campbell, Moray J; Lewy, Greg; Eggo, Margaret C; Loubiere, Laurence S; Franklyn, Jayne A; Boelaert, Kristien; McCabe, Christopher J (2010)
Languages: English
Types: Article
Subjects: Article
Identifiers:pmc:PMC2875163
PTTG Binding Factor (PBF; PTTG1IP) is a relatively uncharacterized oncoprotein whose function remains obscure. Because of the presence of putative oestrogen response elements (ERE) in its promoter, we assessed PBF regulation by oestrogen. PBF mRNA and protein expression were induced by both diethylstilbestrol and 17ß-estradiol in oestrogen receptor alpha (ERα) positive MCF-7 cells. Detailed analysis of the PBF promoter showed that the region −399 to −291 relative to the translational start site contains variable repeats of an 18 bp sequence housing a putative ERE half-site (gcccctcGGTCAcgcctc). Sequencing the PBF promoter from 122 normal subjects revealed that subjects may be homozygous or heterozygous for between 1 and 6 repeats of the ERE. ChIP and oligonucleotide pull down assays revealed ERα binding to the PBF promoter. PBF expression was low or absent in normal breast tissue, but was highly expressed in breast cancers. Subjects with greater numbers of ERE repeats demonstrated higher PBF mRNA expression, and PBF protein expression positively correlated with ERα status. Cell invasion assays revealed that PBF induces invasion through Matrigel, an action that could be abrogated both by siRNA treatment and specific mutation. Further, PBF is a secreted protein, and loss of secretion prevents PBF inducing cell invasion. Given that PBF is a potent transforming gene, we propose that oestrogen treatment in post-menopausal women may up-regulate PBF expression, leading to PBF secretion and increased cell invasion. Further, the number of ERE half sites in the PBF promoter may significantly alter the response to oestrogen treatment in individual subjects.

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