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Updated: Apr 9, 2026

Profiling of Estrogen-regulated MicroRNAs in Breast Cancer Cells
Published on: February 21, 2014
MicroRNA: The Potential Regulator of Endometrial Carcinogenesis
Emmanuel N Kontomanolis, Michael I Koukourakis1
1Department of Radiotherapy and Oncology, Democritus University of Thrace, Alexandroupolis 68100, Greece. mek-2@otenet.gr.
Abstract:
MicroRNAs (miRNAs) are small stable endogenous RNAs, found in all complex organisms and considered by nature as inhibitors of mRNA translation. This class of small posttranscriptional regulatory RNAs originates from the random formation of hairpin precursors in "non-coding" DNA regions; their main function is the control of gene expression status. The premature forms of the fullydeveloped microRNAs are the pre-microRNAs; molecules composed of thousands of nucleotides and constitute 1-2% of the human genome; the human genome encodes at least 1,500 miRNAs. miRNAs do not encode for any proteins; they guide gene modulation and affect crucial biological processes such as cell proliferation, tissue differentiation, apoptosis, cancer progression and female physiology. miRNAs are detected in specific tumor types and seem to be effectively involved in invasion, metastasis and acquire a role in clinical prognosis. miRNA expression is the vital key in cancer cell dysregulation. Cancer cells present with abnormal growth and lack of their apoptosis fate. Normal and neoplastic tissues have dissimilar expression patterns. Endometrial cancer subtypes are outlined by an irregular miRNA expression, along with other human malignancies. miRNAs retain manifold roles in angiogenesis; have a bidirectional impact on oncogenes and tumor suppressor genes in the steps of endometrial cancer growth, being positive or negative regulators of metastasis. The scientific significance of this new class of noncoding RNAs is gradually comprehended. The current review summarizes our knowledge on the role of miRNA in endometrial cancer development and clinical behavior; it outlines the biological pathways strictly modulated by them.
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