Lncrnas and micrornas as essential regulators of stemness in breast cancer stem cells
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Breast cancer is an aggressive disease with a high incidence in women worldwide. Two decades ago, a controversial hypothesis was proposed that cancer arises from a subpopu-lation of “tumor initiating cells” or “cancer stem cells-like” (CSC). Today, CSC are defined as small subset of somatic cancer cells within a tumor with self-renewal properties driven by the aberrant expression of genes involved in the maintenance of a stemness-like phenotype. The understanding of the underlying cellular and molecular mechanisms involved in the maintenance of CSC subpopula-tion are fundamental in the development and persistence of breast cancer. Nowadays, the hypothesis suggests that genetic and epigenetic alterations give rise to breast cancer stem cells (bCSC), which are responsible for self-renewal, tumor growth, chemoresistance, poor prognosis and low survival in patients. However, the prominence of bCSC, as well as the molecular mechanisms that regulates and promotes the malignant phenotypes, are still poorly understood. The role of non-coding RNAs (ncRNAs), such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) acting as oncogenes or tumor suppressor genes has been recently highlighted by a plethora of studies in breast cancer. These ncRNAs positively or negatively impact on different signaling pathways that govern the cancer hallmarks associated with bCSC, making them attractive targets for therapy. In this review, we present a current summary of the studies on the pivotal roles of lncRNAs and microRNAs in the regulation of genes associated to stemness of bCSC. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
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Breast cancer; Cancer stem cells; LncRNAs; MicroRNAs; Therapy aldehyde dehydrogenase isoenzyme 1; alpha6 integrin; beta catenin; beta1 integrin; beta3 integrin; CD133 antigen; CD22 antigen; CD24 antigen; CD34 antigen; cell marker; common acute lymphoblastic leukemia antigen; epidermal growth factor receptor; Hermes antigen; HOTAIR; immunoglobulin enhancer binding protein; leukemia inhibitory factor receptor; long untranslated RNA; microRNA; microRNA 10b; microRNA 200; microRNA 21; microRNA 31; microRNA 34a; octamer transcription factor 4; progesterone receptor; programmed death 1 receptor; protein kinase B; protein p21; protein p53; Smad2 protein; Smad3 protein; Smad4 protein; small interfering RNA; stromal cell derived factor 1; tamoxifen; Thy 1 membrane glycoprotein; transcription factor Sox2; transcriptome; transforming growth factor beta; unclassified drug; vimentin; Wnt protein; long untranslated RNA; microRNA; angiogenesis; apoptosis; Article; breast cancer; cancer growth; cancer inhibition; cancer stem cell; cancer survival; cancer therapy; carcinogenesis; carcinogenicity; cell adhesion; cell cycle arrest; cell differentiation; cell invasion; cell migration; cell proliferation; cell survival; chemosensitivity; cytotoxicity; DNA methylation; down regulation; epigenetics; epithelial mesenchymal transition; gene expression; hedgehog signaling; hippo signaling; immunophenotyping; incidence; JAK-STAT signaling; liposomal delivery; mammary gland; MCF-7 cell line; MDA-MB-231 cell line; menstrual cycle; morphogenesis; mTOR signaling; natural killer cell; Notch signaling; nuclear reprogramming; oncogene c myc; phenotype; protein expression; protein function; protein phosphorylation; radiosensitivity; signal transduction; TGF beta signaling; tumor associated leukocyte; tumor growth; tumor microenvironment; tumor resistance; tumor suppressor gene; tumor volume; upregulation; Wnt signaling; breast tumor; cancer stem cell; cytology; female; gene expression regulation; genetics; human; metabolism; pathology; Breast Neoplasms; Female; Gene Expression Regulation, Neoplastic; Humans; MicroRNAs; Neoplastic Stem Cells; RNA, Long Noncoding
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