International Journal of Molecular Sciences (May 2022)

Role of miRNAs in Human T Cell Leukemia Virus Type 1 Induced T Cell Leukemia: A Literature Review and Bioinformatics Approach

  • Caio Bezerra Machado,
  • Leidivan Sousa da Cunha,
  • Jersey Heitor da Silva Maués,
  • Flávia Melo Cunha de Pinho Pessoa,
  • Marcelo Braga de Oliveira,
  • Rodrigo Monteiro Ribeiro,
  • Germison Silva Lopes,
  • Manoel Odorico de Moraes Filho,
  • Maria Elisabete Amaral de Moraes,
  • André Salim Khayat,
  • Caroline Aquino Moreira-Nunes

DOI
https://doi.org/10.3390/ijms23105486
Journal volume & issue
Vol. 23, no. 10
p. 5486

Abstract

Read online

Human T cell leukemia virus type 1 (HTLV-1) was identified as the first pathogenic human retrovirus and is estimated to infect 5 to 10 million individuals worldwide. Unlike other retroviruses, there is no effective therapy to prevent the onset of the most alarming diseases caused by HTLV-1, and the more severe cases manifest as the malignant phenotype of adult T cell leukemia (ATL). MicroRNA (miRNA) dysfunction is a common feature of leukemogenesis, and it is no different in ATL cases. Therefore, we sought to analyze studies that reported deregulated miRNA expression in HTLV-1 infected cells and patients’ samples to understand how this deregulation could induce malignancy. Through in silico analysis, we identified 12 miRNAs that stood out in the prediction of targets, and we performed functional annotation of the genes linked to these 12 miRNAs that appeared to have a major biological interaction. A total of 90 genes were enriched in 14 KEGG pathways with significant values, including TP53, WNT, MAPK, TGF-β, and Ras signaling pathways. These miRNAs and gene interactions are discussed in further detail for elucidation of how they may act as probable drivers for ATL onset, and while our data provide solid starting points for comprehension of miRNAs’ roles in HTLV-1 infection, continuous effort in oncologic research is still needed to improve our understanding of HTLV-1 induced leukemia.

Keywords