Abstract
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.
Highlights
TMED2 is a member of the tranmembrane emp24 domain [1, 2]
We observed an increased expression of TMED2 in epithelial ovarian carcinoma compared with the normal ovarian tissues
We found that the elevated expression of TMED2 in epithelial ovarian carcinoma promoted proliferation and invasion
Summary
TMED2 is a member of the tranmembrane emp domain [1, 2]. TMED2 was involved in the development of mouse embryos [3]. Previous study reported that ectopic expression of TMED2 can accelerate the proliferation in MC3T3-E1 cell [4]. This indicated its possible role in cancer cells proliferation. The role of TMED2 in epithelial ovarian carcinoma is still unknown. It is often increased expression in many cancers. IGF signaling pathway mediates protease secretion, hypoxia signaling, cancer cell motility and adhesion. Activate IGF2/PI3K/AKT signaling pathway promotes glioblastoma multiforme progression [7]. The role of TMED2 in IGF2/IGF1R/PI3K/AKT pathway is not elucidated yet
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
