OPM-2

Increased Adhesion of OPM-2 Cells to HUVECs After Treatment With CSP

The molecular mechanism underlying the interaction between myeloma cells and stromal cells was investigated by using a human myeloma cell line (OPM-2) and human umbilical vein endothelial cells (HUVECs). Adhesion of OPM-2 cells to HUVECs was found to be significantly augmented with the treatment of OPM-2 cells with an α-glycosidase inhibitor, castanospermine (CSP).

OPM-2 cells were cultured with or without CSP (200 μg/mL) for 48 hours and then cocultured with HUVECs. In the absence of CSP treatment, 17.8% of OPM-2 cells adhered to HUVECs (Fig. 1). The preincubation of OPM-2 cells with CSP led to a significant increase in adhesion of OPM-2 cells, and 24.6% of OPM-2 cells were found to adhere to HUVECs (Fig. 1). The effect of CSP on surface expression of adhesion molecules was examined, which were known to express on myeloma cells. Flow cytometry analysis showed that CD44 and CD49d were expressed on OPM-2 cells at a high level, and CD54 at a moderate level, whereas little or no expression of CD11a, CD18, CD49e, or LAM-1 was observed on the cells (Table 1). The surface expression of the adhesion molecules was not influenced by the treatment of CSP (Table 1). These results indicated that CSP did not affect the expression of the well-known adhesion molecules and suggested that CSP might influence the function of adhesion molecules by altering their oligosaccharide structures.

Fig. 1 Effect of CSP on the adhesion of OPM-2 cells to HUVECs. (Nishiura T, et al., 1996)

Table 1. Effect of CSP treatment on surface expression of adhesion molecules.

MSCs Inhibit the Effects of Dexamethasone on Multiple Myeloma Cells

Mesenchymal stem cells (MSCs) participate in the occurrence and development of multiple myeloma. Multiple myeloma cells (OPM-2 and RPMI8226 cells) were cocultured with MSCs with or without dexamethasone. Treatment with dexamethasone (10 μM) significantly decreased the cell viability of OPM-2 and RPMI8226 cells (Fig. 2a and 2b). However, the presence of MSCs increased the cell viability of OPM-2 and RPMI8226 cells as compared to the dexamethasone-treated cells (Fig. 2a and 2b). Treatment with dexamethasone (10 μM) significantly decreased the cell number and colony number, respectively (Fig. 2c-f). Interestingly, the presence of MSCs increased the cell and colony numbers of OPM-2 and RPMI8226 cells as compared to the dexamethasone-treated cells (Fig. 2c-f).

Treatment with dexamethasone (10 μM) significantly increased the percentage of apoptotic OPM-2 and RPMI8226 cells (Fig. 3a and 3b). However, the presence of MSCs decreased the percentage of apoptotic OPM-2 and RPMI8226 cells as compared to the dexamethasone-treated cells (Fig. 3a and 3b). Moreover, cells were arrested at the G0/G1 phase in the dexamethasone (10 μM)-treated group (Fig. 3c and 3d). Interestingly, the presence of MSCs increased the percentage of cells in the S phase, while decreasing the percentage of cells in the G0/G1 phase.

Fig. 2 The presence of MSCs suppressed the inhibitory effects of dexamethasone on cell proliferation. (Deng M, et al., 2022)

Fig. 3 The presence of MSCs regulated the effects of dexamethasone on cell apoptosis and cell cycle distribution. (Deng M, et al., 2022)