T-cell prolymphocytic leukemia is associated with deregulation of oncogenic microRNAs on transcriptional and epigenetic level.
Paurnima PatilSina HillebrechtEmil ChteinbergCristina LópezUmut H ToprakJulian SeufertStephan H BernhartHelene KretzmerAnke K BergmannSusanne BensJosef HögelAnnika MüllerBilly Michael JebarajAlexandra SchraderPatricia JohanssonDolors CostaMatthias SchlesnerJan DürigMarco HerlingElias CampoStephan StilgenbauerLaura WiehleReiner SiebertPublished in: Genes, chromosomes & cancer (2022)
Deregulation of micro(mi)-RNAs is a common mechanism in tumorigenesis. We investigated the expression of 2083 miRNAs in T-cell prolymphocytic leukemia (T-PLL). Compared to physiologic CD4+ and CD8+ T-cell subsets, 111 miRNAs were differentially expressed in T-PLL. Of these, 33 belonged to miRNA gene clusters linked to cancer. Genomic variants affecting miRNAs were infrequent with the notable exception of copy number aberrations. Remarkably, we found strong upregulation of the miR-200c/-141 cluster in T-PLL to be associated with DNA hypomethylation and active promoter marks. Our findings suggest that copy number aberrations and epigenetic changes could contribute to miRNA deregulation in T-PLL.
Keyphrases
- copy number
- dna methylation
- mitochondrial dna
- genome wide
- gene expression
- poor prognosis
- transcription factor
- cell proliferation
- acute myeloid leukemia
- long non coding rna
- bone marrow
- papillary thyroid
- long noncoding rna
- signaling pathway
- squamous cell
- peripheral blood
- atomic force microscopy
- young adults
- oxidative stress
- childhood cancer