Expression of microRNA-10a, microRNA-342-3p and their predicted target gene TIAM1 in extranodal NK/T-cell lymphoma, nasal type

Abstract

MicroRNAs (miRNAs) may act as oncogenes or tumor suppressor genes in different types of human cancer. T-lymphoma invasion and metastasis inducing factor 1 (TIAM1) participates in the development of several types of human cancer. However, the expression of miRNAs and TIAM1 in extranodal natural killer (NK)/T-cell lymphoma, nasal type (ENKTCL) remains poorly understood. In the present study, the association between the expression levels of miR-10a and miR-342-3p and the protein expression levels of TIAM1 was examined in ENKTCL tissues. The expression levels of miR-10a, miR-22, miR-340, miR-342-3p and miR-590-5p in 15 primary ENKTCL tissues were analyzed using quantitative polymerase chain reaction, and the protein expression levels of TIAM1 in 21 primary ENKTCL tissues were analyzed using immunohistochemistry. The expression levels of miR-10a and miR-342-3p were lower in ENKTCL tissues than in normal NK cells, but no significant differences were observed in the expression levels of miR-22, miR-340 and miR-590-5p in ENKTCL tissues, compared with normal NK cells. The low expression levels of miR-10a detected in the tissues of patients with ENKTCL were inversely correlated with the age of the patients, whereas the low expression levels of miR-342-3p measured in these samples were not correlated with any demographic or clinical features of the patients. The protein expression levels of TIAM1 were higher in ENKTCL tissues than in normal and reactive lymph node hyperplasia tissues, and positively correlated with the Ann Arbor stage and international prognostic index score of the tumors. Furthermore, the expression levels of miRNA-10a and miRNA-342-3p were inversely correlated with the protein expression levels of TIAM1 in ENKTCL tissues. These data suggest that TIAM1 may contribute to the pathogenesis of ENKTCL, and miRNA-10a and miRNA-342-3p may be involved in the development of ENKTCL via the TIAM1 pathway.