Estrogen receptor α variant ERα46 mediates growth inhibition and apoptosis of human HT-29 colon adenocarcinoma cells in the presence of 17β-oestradiol

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Estrogen is involved in suppression of colon cancer development and exerts its function via estrogen receptors α and β (ERα, ERβ). The recently identified ERα46 resulted from exon 1-deletion from the 66-kDa full length form of ERα66 is devoid of the transactivation domain AF-1, whose function remains largely unknown.


In this study, we compared the expression of ERα46 mRNA in 32 normal colorectal tissues and their matched colorectal cancer tissues by real-time quantitative polymerase chain reaction (PCR). Human colon adenocarcinoma cell HT-29, that has low endogenous expression of ERα46, was transfected with ERα46-expression vector; methyl thiazolyl tetrazolium (MTT) assay, flow cytometry, DNA fragmentation and TUNEL staining were used to evaluate the proliferation and apoptosis status of the cells in the presence of 17β-oestradiol.


Higher ERα46 mRNA levels were observed in normal colorectal tissues than in the corresponding cancer tissues. ERα46-transfected cells showed a significantly decreased growth rate than control cells and an accumulation of cells in the G0/1 phase and a reduced proportion of cells in G2/M phase after exposed to 10−8 mol/L 17β-oestradiol. There were also more positive TUNEL stained cells in ERα46-transfected cells than the control cells in the presence of 17β-oestradiol (P<0.05).


These data suggest that ERα46 may be involved in the development and/or progression of colorectal cancer via mediating growth inhibition and apoptosis of cancer cells in the presence of 17β-oestradiol.


Chin Med J 2008;121(11):1025–1031

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