The Role of Immune Modulatory MicroRNAs in Tumors

Abstract

Tumors could evade the control of CD8 + T and/or NK cell-mediated surveillance by distinct immune escape strategies. These include the aberrant expression of HLA class I antigens, coinhibitory or costimulatory molecules, and components of the interferon (IFN) signal transduction pathway. In addition, alterations of the tumor microenvironment could interfere with a proper antitumoral immune response by downregulating or inhibiting the frequency and/or activity of immune effector cells and professional antigen presenting cells. Based on the identification as major mediators of the posttranscriptional silencing of gene expression, microRNAs (miRNAs) have been suggested to play a key role in many biological processes known to be involved in neoplastic transformation. Indeed, miRNA expression is frequently deregulated in many cancer types and could have tumor-suppressive as well as oncogenic potential. This review focused on the characterization of miRNAs, which are involved in the control of the immune surveillance or immune escape of tumors and their use as potential diagnostic and prognostic biomarkers as well as therapeutic targets. Moreover, miRNAs can have dual activities by affecting the neoplastic and immunogenic phenotype of tumors.

Identification of miR-200a-5p targeting the peptide transporter TAP1 and its association with the clinical outcome of melanoma patients

“…60 Functional in vitro and/or in vivo testing of some deregulated miRs suggested potential contributions of specific miRs to the molecular complexity of this malignancy. 61 The miR-200 family is known for its role in cancer metastasis by inhibiting epithelial-mesenchymal transition and differentially regulating morphological plasticity and mode of melanoma cell invasion. 62 The expression of three family members, miR-200a, miR-200b and miR-429, is upregulated in three epithelial cancers (breast, ovarian and melanoma) as determined by high-resolution array based comparative genomic hybridization.…”

“… 60 Functional in vitro and/or in vivo testing of some deregulated miRs suggested potential contributions of specific miRs to the molecular complexity of this malignancy. 61 …”