MiR-338-5p sensitizes glioblastoma cells to radiation through regulation of genes involved in DNA damage response

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00066251" target="_blank" >RIV/00159816:_____/16:00066251 - isvavai.cz</a>

Alternative codes found

RIV/00216224:14740/16:00088839 RIV/65269705:_____/16:00066251 RIV/00843989:_____/16:E0105477 RIV/00209805:_____/16:N0000054

Result on the web

<a href="http://dx.doi.org/10.1007/s13277-015-4654-x" target="_blank" >http://dx.doi.org/10.1007/s13277-015-4654-x</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s13277-015-4654-x" target="_blank" >10.1007/s13277-015-4654-x</a>

Result language

angličtina

Original language name

MiR-338-5p sensitizes glioblastoma cells to radiation through regulation of genes involved in DNA damage response

Original language description

Glioblastoma multiforme (GBM) is the most aggressive form of brain tumor. Despite radical surgery and radiotherapy supported by chemotherapy, the disease still remains incurable with an extremely low median survival rate of 12-15 months from the time of initial diagnosis. The main cause of treatment failure is considered to be the presence of cells that are resistant to the treatment. MicroRNAs (miRNAs) as regulators of gene expression are involved in the tumor pathogenesis, including GBM. MiR-338 is a brain-specific miRNA which has been described to target pathways involved in proliferation and differentiation. In our study, miR-338-3p and miR-338-5p were differentially expressed in GBM tissue in comparison to non-tumor brain tissue. Overexpression of miR-338-3p with miRNA mimic did not show any changes in proliferation rates in GBM cell lines (A172, T98G, U87MG). On the other hand, pre-miR-338-5p notably decreased proliferation and caused cell cycle arrest. Since radiation is currently the main treatment modality in GBM, we combined overexpression of pre-miR-338-5p with radiation, which led to significantly decreased cell proliferation, increased cell cycle arrest, and apoptosis in comparison to irradiation-only cells. To better elucidate the mechanism of action, we performed gene expression profiling analysis that revealed targets of miR-338-5p being Ndfip1, Rheb, and ppp2R5a. These genes have been described to be involved in DNA damage response, proliferation, and cell cycle regulation. To our knowledge, this is the first study to describe the role of miR-338-5p in GBM and its potential to improve the sensitivity of GBM to radiation.

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

FD - Oncology and haematology

OECD FORD branch

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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

Publication year

2016

Confidentiality

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

Name of the periodical

Tumor Biology

ISSN

1010-4283

e-ISSN

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Volume of the periodical

37

Issue of the periodical within the volume

6

Country of publishing house

NL - THE KINGDOM OF THE NETHERLANDS

Number of pages

9

Pages from-to

7719-7727

UT code for WoS article

000376464700071

EID of the result in the Scopus database

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