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miR-150 downregulation contributes to the high-grade transformation of follicular lymphoma by upregulating FOXP1 levels

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064203%3A_____%2F18%3A10427541" target="_blank" >RIV/00064203:_____/18:10427541 - isvavai.cz</a>

  • Alternative codes found

    RIV/65269705:_____/18:00069101 RIV/00216224:14740/18:00105661 RIV/00216208:11110/18:10384245 RIV/00216208:11120/18:43917064 and 3 more

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=U4~iq_oMNU" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=U4~iq_oMNU</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1182/blood-2018-06-855502" target="_blank" >10.1182/blood-2018-06-855502</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    miR-150 downregulation contributes to the high-grade transformation of follicular lymphoma by upregulating FOXP1 levels

  • Original language description

    Follicular lymphoma (FL) is a common indolent B-cell malignancy with a variable clinical course. An unfavorable event in its course is histological transformation to a high-grade lymphoma, typically diffuse large B-cell lymphoma. Recent studies show that genetic aberrations ofMYC or its overexpression are associated with FL transformation (tFL). However, the precise molecular mechanisms underlying tFL are unclear. Here we performed the first profiling of expression of microRNAs (miRNAs) in paired samples of FL and tFL and identified 5 miRNAs as being differentially expressed. We focused on one of these miRNAs, namely miR-150, which was uniformly downmodulated in all examined tFLs (similar to 3.5-fold), and observed that high levels of MYC are responsible for repressing miR-150 in tFL by binding in its upstream region. This MYC-mediated repression of miR-150 in B cells is not dependent on LIN28A/B proteins, which influence the maturation of miR-150 precursor (pri-miR-150) in myeloid cells. We also demonstrated that low miR-150 levels in tFL lead to upregulation of its target, namely FOXP1 protein, which is a known positive regulator of cell survival, as well as B-cell receptor and NF-kappa B signaling in malignant B cells. We revealed that low levels of miR-150 and high levels of its target, FOXP1, are associated with shorter overall survival in FL and suggest that miR-150 could serve as a good biomarker measurable in formalin-fixed paraffin-embedded tissue. Overall, our study demonstrates the role of theMYC/miR-150/FOXP1 axis in malignant B cells as a determinant of FL aggressiveness and its high-grade transformation.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30205 - Hematology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Blood

  • ISSN

    0006-4971

  • e-ISSN

  • Volume of the periodical

    132

  • Issue of the periodical within the volume

    22

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    12

  • Pages from-to

    2389-2400

  • UT code for WoS article

    000451634400012

  • EID of the result in the Scopus database

    2-s2.0-85057234268