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

Background Estrogen is involved in suppression of colon cancer development and exerts its function via estrogen receptors alpha and beta (ER alpha, ER beta). The recently identified ER alpha 46 resulted from exon 1-deletion from the 66-kDa full length form of ER alpha 66 is devoid of the transactivation domain AF-1, whose function remains largely unknown. Methods In this study, we compared the expression of ERa46 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 ERa46, was transfected with ER alpha 46-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 17 beta-oestradiol. Results Higher ERa46 mRNA levels were observed in normal colorectal tissues than in the corresponding cancer tissues. ER alpha 46-transfected cells showed a significantly decreased growth rate than control cells and an accumulation of cells in the G(0/1) phase and a reduced proportion of cells in G(2)/M phase after exposed to 10(-8) mol/L 17 beta-oestradiol. There were also more positive TUNEL stained cells in ERa46-transfected cells than the control cells in the presence of 17 beta-oestradiol (P < 0.05). Conclusions These data suggest that ER alpha 46 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 17 beta-oestradiol.