The steroid hormone 17β-estradiol (E2) regulates a number of developmental and physiological processes. The classical understanding of the estrogen signaling implies that the two nuclear receptors (ER), ERα and ERβ, mediate all the physiological responses of E2. ERs are transcription factors, which regulate the expression of their targets upon binding to E2. Estrogens also mediate a lot of rapid outcomes within a matter of seconds to minutes that cannot be explained by the classical understanding of estrogen signaling, which involves transcription of target genes mediated by the ERs. Whereas, many of the rapid effects of estrogen are attributed to the cytoplasmic pools of ERs, it has become clear in the recent years that there are other factors contributing to the rapid effects of estrogen and one of the emerging such factors is a G-protein coupled receptor, GPR30. MicroRNAs (miRNAs) are a new class of small non-coding RNAs, 20 to 25 nucleotides in length that regulate the expression of other genes. Upon binding the 3' untranslated region (UTR) of target mRNAs, miRNAs typically reduce their stability and/or translation. miRNAs are shown to be involved in regulating virtually every cellular process and their deregulation has been shown to contribute to many diseases. There are nearly 1,000 different miRNAs in humans, which regulate expression of thousands of other genes, reflecting that this is indeed a major layer of gene expression regulation. In my PhD, I had focused on these two different themes of estrogen signaling. In the first project, using a DNA microarray approach, we identified the target genes of the emerging new player in estrogen signaling, GPR30. In the second part, we have addressed some previously unexplained observations about the role of the 3ʼUTR of the ERα mRNA in regulating ERα levels and estrogen signaling.