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MicroRNA-126 Suppresses Mesothelioma Malignancy by Targeting IRS1 and Interfering with the Mitochondrial Function

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F14%3A00437289" target="_blank" >RIV/86652036:_____/14:00437289 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1089/ars.2013.5215" target="_blank" >http://dx.doi.org/10.1089/ars.2013.5215</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1089/ars.2013.5215" target="_blank" >10.1089/ars.2013.5215</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    MicroRNA-126 Suppresses Mesothelioma Malignancy by Targeting IRS1 and Interfering with the Mitochondrial Function

  • Original language description

    MiR126 was found to be frequently lost in many types of cancer, including malignant mesothelioma (MM), which represents one of the most challenging neoplastic diseases. In this study, we investigated the potential tumor suppressor function of MiR126 in MM cells. The effect of MiR126 was examined in response to oxidative stress, aberrant mitochondrial function induced by inhibition of complex I, mitochondrial DNA (mtDNA) depletion, and hypoxia. Results: MiR126 was up-regulated by oxidative stress in nonmalignant mesothelial (Met5A) and MM (H28) cell lines. In Met5A cells, rotenone inhibited MiR126 expression, but mtDNA depletion and hypoxia up-regulated MiR126. However, these various stimuli suppressed the levels of MiR126 in H28 cells.MiR126 affected mitochondrial energy metabolism, reduced mitochondrial respiration, and promoted glycolysis in H28 cells.This metabolic shift, associated with insulin receptor substrate-1 (IRS1)-modulated ATP-citrate lyase deregulation,resulted in higher

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2014

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Antioxidants & Redox Signaling

  • ISSN

    1523-0864

  • e-ISSN

  • Volume of the periodical

    21

  • Issue of the periodical within the volume

    15

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    17

  • Pages from-to

    2109-2125

  • UT code for WoS article

    000343982000004

  • EID of the result in the Scopus database