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In human, estrogens play important roles in many physiological processes, and is also found to be
connected with numerous cancers. In these diseases, estrogen mediates its effects through the estrogen
receptor (ER), which serves as the basis for many current clinical diagnosis. Two forms of the estrogen
receptor have been identified, ERα and ERβ, and show different and specific functions. The two estrogen
receptors belong to a family of ligand-regulated transcription factors. Estrogen via ERα stimulates
proliferation in the breast, uterus, and developing prostate, while estrogen via ERβ inhibits proliferation and
promotes differentiation in the prostate, mammary gland, colon, lung, and bone marrow stem cells.
MicroRNAs (miRs) are small non-coding RNA molecules that occur naturally and downregulate protein
expression by translational blockade of the target mRNA or by promoting mRNA decay. MiR-21 is one of the
most studied miRNAs in cancers. MiR-21 is overexpressed in the most solid tumors, promoting progression
and metastasis. The miR-21 gene is located on the chromosome 17, in the 10th intron of a protein-coding gene,
TMEM49. While, the function of TMEM49 is currently unknown. Our experiment is designed to identity the
relationship between miR-21 and ERβ in cancer progression. The human cancer cells were transfected with
ERβ. Real-time PCR analysis showed that the expression level of miR-21 was significantly inhibited down by
ERβ treatment. As MTT assay showed the tumor cell survival rate was also inhibited significantly. Go/Gl
phase cell cycle arrest was founded and tumor cell apoptosis was induced in ERβ group.
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