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miR-125b Upregulates miR-34a and Sequentially Activates Stress Adaption and Cell Death Mechanisms in Multiple Myeloma

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62157124%3A16810%2F19%3A43877678" target="_blank" >RIV/62157124:16810/19:43877678 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11130/19:10394757

  • Result on the web

    <a href="https://www.sciencedirect.com/science/article/pii/S216225311930054X" target="_blank" >https://www.sciencedirect.com/science/article/pii/S216225311930054X</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.omtn.2019.02.023" target="_blank" >10.1016/j.omtn.2019.02.023</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    miR-125b Upregulates miR-34a and Sequentially Activates Stress Adaption and Cell Death Mechanisms in Multiple Myeloma

  • Original language description

    miR-125b, ubiquitously expressed and frequently dysregulated in several tumors, has gained special interest in the field of cancer research, displaying either oncogenic or oncosuppressor potential based on tumor type. We have previously demonstrated its tumor-suppressive role in multiple myeloma (MM), but the analysis of molecular mechanisms needs additional investigation. The purpose of this study was to explore the effects of miR-125b and its chemically modified analogs in modulating cell viability and cancer-associated molecular pathways, also focusing on the functional aspects of stress adaptation (autophagy and senescence), as well as programmed cell death (apoptosis). Based on the well-known low microRNA (miRNA) stability in therapeutic application, we designed chemically modified miR-125b mimics, laying the bases for their subsequent investigation in in vivo models. Our study clearly confirmed an oncosuppressive function depending on the repression of multiple targets, and it allowed the identification, for the first time, of miR-125b-dependent miR-34a stimulation as a possible consequence of the inhibitory role on the interleukin-6 receptor (IL-6R)/signal transducer and activator of transcription 3 (STAT3)/miR-34a feedback loop. Moreover, we identified a pattern of miR-125b-co-regulated miRNAs, shedding light on possible new players of anti-MM activity. Finally, functional studies also revealed a sequential activation of senescence, autophagy, and apoptosis, thus indicating, for the first two processes, an early cytoprotective and inhibitory role from apoptosis activation.

  • 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

    40301 - Veterinary science

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2019

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Molecular Therapy-Nucleic Acids

  • ISSN

    2162-2531

  • e-ISSN

  • Volume of the periodical

    16

  • Issue of the periodical within the volume

    19

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    16

  • Pages from-to

    391-406

  • UT code for WoS article

    000470250900035

  • EID of the result in the Scopus database