Journal
ONCOTARGET
Volume 8, Issue 55, Pages 94151-94165Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.21593
Keywords
epithelial ovarian cancer; TMED2; IGF1R; AKT; miR-30a
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Funding
- Science and Technology Program Project of Guangdong Province [2016A020215115]
- Special Funding for Production-Study-Research Cooperative Innovation Program of Huadu District, Guangzhou [HD15CXY006]
- Major Project for Health Care of Tianhe District, Guangzhou [201604KW010]
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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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