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The Role of Micrornas in Oral Squamous Cell Carcinoma Pathogenesis: a Literature Review

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The Role of Micrornas in Oral Squamous Cell Carcinoma Pathogenesis: a Literature Review Applied Cancer Research. 2013;33(4):198-205. REVIEW The role of microRNAS in oral squamous cell carcinoma pathogenesis: a literature review Anne Maria Guimarães Lessa1, Ludmila Faro Valverde2, Rosane Borges Dias2, Maria Cecília Mathias Machado1, Jean Nunes dos Santos3, Clarissa Araújo Gurgel Rocha3 ABSTRACT In this review, we summarize the main aspects related to the involvement of microRNAs (miRNAs) in oral carcinogenesis. miRNAs are small non-protein-coding RNAs that function such as regulators of gene expression. They regulate various biological processes such as growth, differentiation and apoptosis and have been widely studied in carcinogenesis. miRNAs may exhibit oncogenic or tumor suppressor activity in cancer, depending on the biological context and the cell type. The altered expression patterns of miRNA in cancer could serve as molecular biomarkers for tumor diagnosis, prognosis and disease-specific prediction of therapeutic responses. The literature indicates that up-regulation of miR-21, miR-221, miR-184 and under expression of miR-133a, miR-375 and let-7b are the principal profile in oral squamous cell carcinomas. Keywords: gene expression; microRNAS; MIRN133 microRNA, human; MIRN184 microRNA, human; MIRN21 microRNA, human; MIRN221 microRNA, human; MIRN375 microRNA, human; mirnlet7 microRNA, human; mouth mucosa; mouth neoplasms; tumor markers, biological. INTRODUCTION years later, Reinhart et al.12 observed that another C. elegans heterochronic gene, let-7, was also represented by a small Cells have developed several biological mechanisms to non-coding RNA capable of starting the temporal cascade of ensure that mitosis, differentiation and death occur in a coor- regulatory genes through an RNA-RNA interaction with the 3 dinated manner and disturbances in genes related with these untranslated region (UTR) of target genes. This discovery 1 cellular processes could result in tumor initiation and cancer . prompted scientists to investigate other small non-coding The mechanisms responsible for the human cancer patho- RNAs in various organisms and cellular systems. genesis are not fully identified, despite advances in molecular The identification of hundreds of miRNAs in worm, biology. However, researchers have identified small molecules animal and plant genomes has now attracted the attention of of non-coding RNA, called microRNAs (miRNAs) which can many researchers10,13-15. It is estimated that miRNAs comprise 2-5 function as tumor suppressor genes and/or oncogenes . 1-4% of all human genes, which makes miRNAs one of MiRNAs are small non-coding and single-stranded the largest regulators of gene expression16. Many miRNAs RNAs involved in numerous physiological and pathological are evolutionarily conserved from worms to humans, processes. They are a post-transcriptional regulators with implying that these miRNAs run essential processes during approximately 20 to 22 nucleotides that bind to comple- development and adult life, such as cellular development, mentary messenger RNAs sequences, usually resulting in proliferation migration, differentiation, and apoptosis1,9. 2,3,6-10 their silencing . In fact, miRNAs negatively regulate Another important property is the fact that only one 4,7 gene expression at a post-transcriptional leve . miRNA can target hundreds of different mRNAs, suggesting The first miRNA was identified in Caenorhabditis that miRNAs might act to regulate mRNA translation and elegans and named lin-4, in 1993. This miRNA controls the turnover7. To date, more than 2000 mature miRNAs have 11 timing and progression of the nematode life cycle . Seven been described in humans, and many of them have been identified to have an important role in disease progression4. 1 Undergraduate student - (Undergraduate student). It has also been estimated that more than 60% of human 2 Master Student - (Master Student). 2,17 3 PhD - (PhD). protein-coding genes are regulated by miRNAs . Previous studies have indicated that miRNAs may Send correspondence to: 1,18-21 Federal University of Bahia. participate in tumorigenesis and affect the etiology, Clarissa Araújo Gurgel Rocha. diagnosis, and prognosis of various cancers1,22-28. Moreover, Av. Araújo Pinho, nº 62. Salvador - BA. Brazil. CEP: 40110-150 the miRNAs may be involved in regulation of the immune Email: [email protected] and inflammatory response systems29,30, becoming Submitted: 09/15/2013 attractive molecules as markers as well as for prediction Aproved: 12/06/2013 of therapy response and surveillance of cancer31. Applied Cancer Research, Volume 33, Number 4, 2013 199 Oncogenic miRNAs are found in malignant tumors and could act by stimulating cellular proliferation or inhibiting the action of tumor suppressor genes and genes that control apoptosis2,3,32,33. Some miRNAs have reduced expression in malignant tumors and are considered tumor suppressors. These miRNAs work against the development of cancer by inhibiting oncogenes3,32. In oral cancer, some studies demonstrated up and down-regulated miRNAs indicating that these molecules may participate in the molecular mechanisms involved in this tumor. Thus, this review aimed to provide an overview about miRNA and describe evidences of the potential participation of miRNAs in oral carcinogenesis. miRNA - Biogenesis Most miRNA-coding genes are located in intergenic Figure 1. Biogenesis of miRNAs. MicroRNA (miRNA) genes are generally regions and its biogenesis is controlled by two RNA-dependent transcribed by RNA Polymerase II (Pol II) in the nucleus to form large pri-miRNA enzymes, which convert a long primary transcript into a mature transcripts. These pri-miRNA transcripts are processed by the RNase III enzyme miRNA7. Drosha and its co-factor, Pasha, to release the ~70-nucleotide pre-miRNA miRNA biogenesis is a complex multi-step process that precursor product. RAN-GTP and exportin 5 transport the pre-miRNA into involves different cellular compartments. This process starts the cytoplasm. Subsequently, another RNase III enzyme, Dicer, processes the pre-miRNA to generate a transient ~22-nucleotide miRNA: miRNA* duplex. in the nucleus, where miRNAs are encoded by genomic DNA The mature miRNA strand is preferably retained in the RNA-induced silencing and transcribed by a RNA polymerase II into the long primary complex (miRISC) and the complementary strand undergoes destruction. transcript called pri-miRNAs5,9. The pri-miRNAs form secondary The mature miRNA then binds to complementary sites in the mRNA target structures named as “stem” regions2,6,34 and are processed in the to negatively regulate gene expression in one of two mechanisms: mRNA nucleus in pre-miRNAs containing 70 nucleotides by a complex degradation/cleavage or repression of translation of mRNA. formed by the RNase III enzyme (Drosha) and a double strand RNA binding protein (named Pasha or DGCR8)2,6,35. The characteristics, such as loss of cellular identity, increased pre-miRNAs are then exported to the cytoplasm by exportin capacity to grow and proliferate as well as alterations in 5 and submitted to an additional processing step in which a systems that control cellular death. Studies in a variety miRNA duplex is excised by another RNase III enzyme (Dicer). of organisms revealed that miRNAs have the capacity to Subsequently, the miRNA duplex is incorporated to the RNA- regulate these cellular processes, corroborating to cancer induced silencing complex (miRISC) and the complementary pathogenesis. miRNAs lin-4 and let-7, for example, have strand undergoes destruction5,6,34. The mature miRNA strand been related to control duration of the development of 36 is preferably retained in the miRISC complex and regulates its C. elegans , and mutations in these miRNAs results in target genes1 through two mechanisms: mRNA degradation abnormalities in cell cycle and cellular differentiation, or repression of translation of mRNA6,32, depending on the preventing cells from reaching a complete differentiated 33 degree of complementarity between the bases of the miRNA state . In addition, because each miRNA regulates and mRNA35. Figure 1 illustrates the biogenesis of miRNAs. the expression of hundreds of different genes, miRNAs can Studies on the biogenesis of the miRNA pathways function as master coordinators, efficiently regulating and 2 have shown that the miRNAs expression is regulated at coordinating multiple cellular pathways and processes . three different levels, including transcription, processing The role of miRNA in tumorigenesis was first 37 and subcellular localization. The regulation of pri-miRNA reported by Calin et al. in chronic lymphocytic transcription is one of the most relevant mechanisms leukemia (CLL). Ever since, there has been an explosion modulating miRNA abundance, by the action of several of publications showing miRNA deregulation in various factors including transcription factors, silencers, enhancers cancer types 2. Recent studies have shown that over and epigenetic modification in miRNA promoters. Moreover, 50% of miRNA codifying genes are located in DNA post-transcriptional factors can also modulate the miRNAs regions associated with cancer, corroborating to this 17,32,38 expression, such as p53, histone deacetylase I, and cytokines9. hypothesis . The mechanisms responsible for the alterations in miRNA and Cancer the expression of miRNAs involve epigenetic modifications It is not surprising that miRNA deregulation or mutations in the DNA sequences, such as deletions, 33 is a hallmark of several pathological conditions, substitutions,
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