Knockdown of TMED3 inhibits cell viability and migration and increases apoptosis in human chordoma cells.

ABSTRACT: Chordoma is a rare low‑grade tumor of the axial skeleton. Over previous decades, a range of targeted drugs have been used for treating chordoma, with more specific and effective therapies under investigation. Transmembrane Emp24 protein transport domain containing 3 (TMED3) is a novel gene reported to be a regulator of oncogenesis, cancer development and metastasis; however, its role in chordoma remains unclear. In the present study, the expression of TMED3 was investigated in chordoma cells, and the effect of TMED3 knockdown on chordoma development was examined in vitro and in vivo, followed by exploration of differentially expressed proteins in TMED3‑silenced chordoma cells via an apoptosis antibody array. Reverse transcription‑quantitative PCR and western blot assays were

SUBMITTER: Yang J 

PROVIDER: S-EPMC7949631 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature