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TMED2 promotes epithelial ovarian cancer growth

TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell prolif...

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Autores principales: Shi-Peng, Gong, Chun-Lin, Chen, Huan, Wu, Fan-Liang, Meng, Yong-Ning, Chen, Ya-Di, Zhang, Guang-Ping, Zhang, Ye-Ping, Cai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706863/
https://www.ncbi.nlm.nih.gov/pubmed/29212217
http://dx.doi.org/10.18632/oncotarget.21593
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author Shi-Peng, Gong
Chun-Lin, Chen
Huan, Wu
Fan-Liang, Meng
Yong-Ning, Chen
Ya-Di, Zhang
Guang-Ping, Zhang
Ye-Ping, Cai
author_facet Shi-Peng, Gong
Chun-Lin, Chen
Huan, Wu
Fan-Liang, Meng
Yong-Ning, Chen
Ya-Di, Zhang
Guang-Ping, Zhang
Ye-Ping, Cai
author_sort Shi-Peng, Gong
collection PubMed
description TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell proliferation, migration and invasion. Silencing TMED2 inhibited ovarian cancer growth in mice. Silencing TMED2 inhibited IGF2/IGF1R/PI3K/Akt pathway. In agreement, ectopically expressed TMED2 activated IGF2/IGF1R/PI3K/Akt pathway. Mechanistic study revealed that TMED2 directly binds to AKT2, thereby facilitating its phosphorylation. We also found that TMED2 increased IGF1R expression by competing for miR-30a. Thus, TMED2 is oncogenic and a potential target for epithelial ovarian cancer therapy.
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spelling pubmed-57068632017-12-05 TMED2 promotes epithelial ovarian cancer growth Shi-Peng, Gong Chun-Lin, Chen Huan, Wu Fan-Liang, Meng Yong-Ning, Chen Ya-Di, Zhang Guang-Ping, Zhang Ye-Ping, Cai Oncotarget Research Paper TMED2 is involved in morphogenesis of the mouse embryo and placenta. We found that expression of TMED2 was higher in epithelial ovarian cancer tissues than normal ovarian tissues. Silencing TMED2 decreased cell proliferation, migration, and invasion. Ectopic expression of TMED2 increased cell proliferation, migration and invasion. Silencing TMED2 inhibited ovarian cancer growth in mice. Silencing TMED2 inhibited IGF2/IGF1R/PI3K/Akt pathway. In agreement, ectopically expressed TMED2 activated IGF2/IGF1R/PI3K/Akt pathway. Mechanistic study revealed that TMED2 directly binds to AKT2, thereby facilitating its phosphorylation. We also found that TMED2 increased IGF1R expression by competing for miR-30a. Thus, TMED2 is oncogenic and a potential target for epithelial ovarian cancer therapy. Impact Journals LLC 2017-10-06 /pmc/articles/PMC5706863/ /pubmed/29212217 http://dx.doi.org/10.18632/oncotarget.21593 Text en Copyright: © 2017 Shi-Peng et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Shi-Peng, Gong
Chun-Lin, Chen
Huan, Wu
Fan-Liang, Meng
Yong-Ning, Chen
Ya-Di, Zhang
Guang-Ping, Zhang
Ye-Ping, Cai
TMED2 promotes epithelial ovarian cancer growth
title TMED2 promotes epithelial ovarian cancer growth
title_full TMED2 promotes epithelial ovarian cancer growth
title_fullStr TMED2 promotes epithelial ovarian cancer growth
title_full_unstemmed TMED2 promotes epithelial ovarian cancer growth
title_short TMED2 promotes epithelial ovarian cancer growth
title_sort tmed2 promotes epithelial ovarian cancer growth
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706863/
https://www.ncbi.nlm.nih.gov/pubmed/29212217
http://dx.doi.org/10.18632/oncotarget.21593
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