Conclusion
Based on these results, TMED2 may play an important role in the pathogenesis of MM. This novel study may contribute to further investigations of useful biomarkers and potential therapeutic targets in patients with MM.
Methods
Real-time quantitative PCR (RT-qPCR) was used to detect the expression of TMED2 in MM cell lines, including MM.1S and RPMI 8226 cells, and lentivirus vector-mediated TMED2 gene silencing was used to further study the effect of the downregulation of TMED2 expression on cell viability, the cell cycle, and apoptosis.
Objective
TMED2 is a member of the transmembrane emp24 domain (Tmed)/p24 protein family, which is significantly upregulated in breast cancer, ovarian cancer and other tumour tissues. The purpose of this study was to investigate the expression of TMED2 in MM cell lines and its effect on the biological behaviour of MM cell lines.
Results
Based on the RT-qPCR results, the expression of the TMED2 mRNA was increased in the MM cell lines MM.1S and RPMI 8226 compared with endogenous control GAPDH. The expression of the TMED2 mRNA was substantially reduced after transfection of the shRNA targeting TMED2 (shTMED2) in both MM cell lines. The CCK-8 assay showed significant decreases in the viability of MM.1S and RPMI 8226 cells, suggesting that the TMED2 gene plays an important role in the proliferation of these two cell lines. The cell cycle of MM.1S and RPMI 8226 cells was substantially altered by shTMED2, as evidenced by the increased number of cells in G1 phase and decreased number of cells in S and G2/M phases. The FACS analysis revealed a significant increase in the apoptosis of MM.1S and RPMI 8226 cells due to the increased activity of Caspase 3/7, suggesting that the TMED2 gene is significantly related to the apoptosis of these two cell lines.