miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)

miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)

MicroRNA contribute to tumor radiation resistance, which is an important clinical problem, and thus we are interested in identifying and characterizing their function. We demonstrate that miR-620 contributes to radiation resistance in cancer cells by increasing proliferation, and decreasing the G2/M...

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Main Authors: Huang, Xiaoyong, Taeb, Samira, Jahangiri, Sahar, Korpela, Elina, Cadonic, Ivan, Yu, Nancy, Krylov, Sergey N., Fokas, Emmanouil, Boutros, Paul C., Liu, Stanley K.
Format: Online
Language:English
Published: Impact Journals LLC 2015
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4673174/
id pubmed-4673174
recordtype oai_dc
spelling pubmed-46731742015-12-23 miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD) Huang, Xiaoyong Taeb, Samira Jahangiri, Sahar Korpela, Elina Cadonic, Ivan Yu, Nancy Krylov, Sergey N. Fokas, Emmanouil Boutros, Paul C. Liu, Stanley K. Research Paper MicroRNA contribute to tumor radiation resistance, which is an important clinical problem, and thus we are interested in identifying and characterizing their function. We demonstrate that miR-620 contributes to radiation resistance in cancer cells by increasing proliferation, and decreasing the G2/M block. We identify the hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (HPGD/15-PGDH) tumor suppressor gene as a direct miR-620 target, which results in increased prostaglandin E2 (PGE2) levels. Furthermore, we show that siRNA targeting of HPGD or administration of exogenous PGE2 recapitulates radioresistance. Targeting of the EP2 receptor that responds to PGE2 using pharmacological or genetic approaches, abrogates radioresistance. Tumor xenograft experiments confirm that miR-620 increases proliferation and tumor radioresistance in vivo. Regulation of PGE2 levels via targeting of HPGD by miR-620 is an innovative manner by which a microRNA can induce radiation resistance. Impact Journals LLC 2015-06-04 /pmc/articles/PMC4673174/ /pubmed/26068950 Text en Copyright: © 2015 Huang et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Huang, Xiaoyong
Taeb, Samira
Jahangiri, Sahar
Korpela, Elina
Cadonic, Ivan
Yu, Nancy
Krylov, Sergey N.
Fokas, Emmanouil
Boutros, Paul C.
Liu, Stanley K.
spellingShingle Huang, Xiaoyong
Taeb, Samira
Jahangiri, Sahar
Korpela, Elina
Cadonic, Ivan
Yu, Nancy
Krylov, Sergey N.
Fokas, Emmanouil
Boutros, Paul C.
Liu, Stanley K.
miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)
author_facet Huang, Xiaoyong
Taeb, Samira
Jahangiri, Sahar
Korpela, Elina
Cadonic, Ivan
Yu, Nancy
Krylov, Sergey N.
Fokas, Emmanouil
Boutros, Paul C.
Liu, Stanley K.
author_sort Huang, Xiaoyong
title miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)
title_short miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)
title_full miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)
title_fullStr miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)
title_full_unstemmed miR-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (HPGD)
title_sort mir-620 promotes tumor radioresistance by targeting 15-hydroxyprostaglandin dehydrogenase (hpgd)
description MicroRNA contribute to tumor radiation resistance, which is an important clinical problem, and thus we are interested in identifying and characterizing their function. We demonstrate that miR-620 contributes to radiation resistance in cancer cells by increasing proliferation, and decreasing the G2/M block. We identify the hydroxyprostaglandin dehydrogenase 15-(nicotinamide adenine dinucleotide) (HPGD/15-PGDH) tumor suppressor gene as a direct miR-620 target, which results in increased prostaglandin E2 (PGE2) levels. Furthermore, we show that siRNA targeting of HPGD or administration of exogenous PGE2 recapitulates radioresistance. Targeting of the EP2 receptor that responds to PGE2 using pharmacological or genetic approaches, abrogates radioresistance. Tumor xenograft experiments confirm that miR-620 increases proliferation and tumor radioresistance in vivo. Regulation of PGE2 levels via targeting of HPGD by miR-620 is an innovative manner by which a microRNA can induce radiation resistance.
publisher Impact Journals LLC
publishDate 2015
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4673174/
_version_ 1613510855372046336

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