کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1992856 | 1541063 | 2008 | 5 صفحه PDF | دانلود رایگان |

Estrogen is involved in suppression of colorectal cancer development and exerts its function via estrogen receptors α, β and their splicing variants. Whether the recently indentified ER-α splicing variants, ER-α36 and ER-α46, play a role in colorectal cancer development is unknown. In this study, we quantified the mRNA copy numbers of wild type ER-α (ER-α66), ER-α46 and ER-α36 in 35 colorectal cancers and their matched normal colorectal tissues by quantitative real-time PCR assay, and correlated their mRNA levels with the clinicopathological properties of the tumors. We found that ER-α66, ER-α46 and ER-α36 mRNAs were coexpressed in all colorectal cancers and their matched normal tissues. The decreased mRNA levels of ER-α36 and ER-α46 whereas no difference of ER-α66 mRNA was observed in colorectal cancers compared to their matched normal tissues. Moreover, change in the expression of ER-α36 mRNA level was correlated with Dukes’ stage of the tumor and the lymph node metastasis. ER-α36 mRNA was decreased significantly in Dukes’ C + D compared to Dukes’ A + B stage tumors (P = 0.017), and the expression of ER-α36 mRNA in N1/N2 was lower than that in N0 lymph node metastasis (P = 0.049). So ER-α36 and ER-α46 might be implicated in the development and progression of colorectal cancers.
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 112, Issues 1–3, November 2008, Pages 20–24