Fig. 2

Anti-LSR monoclonal antibody shows a significant antitumor effect against endometrial cancer in a xenograft model. Healthy female 6-week-old nude mice were subcutaneously inoculated with 2.0 X 10⁶ HEC1 cells. When the tumor volume reached approximately 100 mm³, the mice were randomized into two groups (5 mice per group) and administrated with isotype control mouse IgG2a antibody (control Ab) or anti-LSR monoclonal antibody (anti-LSR mAb, #1–25) twice a week for 3 weeks. A Expression of LSR in HEC1-xenograft tumors in nude mice was confirmed by immunohistochemistry. Scale bar, 200 μm. B Anti-LSR mAb significantly inhibited tumor growth compared with the control Ab (mean tumor volume, 407.1 mm³ versus 726.3 mm³, p = 0.019). Data were shown as means ± standard errors of the means (n = 5; *p < 0.05, **p < 0.01). C No significant weight loss was observed in the mice following anti-LSR mAb administration. D The rate of Ki-67-positive cells was significantly decreased in the anti-LSR mAb-treated group compared with the control Ab-treated group (31.1% versus 80.8%, p < 0.01). Magnification, 400 X; Scale bar, 100 μm. Data were shown as means ± standard deviations (n = 5; **p < 0.01). E The rate of cleaved caspase-3-positive cells was significantly increased in the anti-LSR mAb-treated group compared with that in the control Ab-treated group (12.9% versus 2.0%, p < 0.01). These results suggest that our anti-LSR mAb exerts a significant antitumor effect associated with apoptosis in vivo. Magnification, 400 X; Scale bar, 100 μm. Data were shown as means ± standard deviations (n = 5; **p < 0.01)