Treatment with Ang1 and Ang2 inhibitors modulates the phenotype of human tumor cells

A. OV 17-1
HLA-A2CEAMUC-1CD54CalreticulinCD95Trail-R1Trail-R2
% (MFI)% (MFI)% (MFI)% (MFI)% (MFI)% (MFI)% (MFI)% (MFI)
 Control99.4(34250)40.7(731)55.9(1170)93.8(16581)3.5(431)57.2(691)27.4(604)10.1(93)
 mL4-3 + L1-7(N)99.1(34180)40.0(872)59.0(1124)97.0(23584)3.7(429)65.3(813)33.7(750)10.1(107)
B. MDA-MB-231
HLA-A2CEAMUC-1CD54CalreticulinCD95Trail-R1Trail-R2
% (MFI)% (MFI)%(MFI)% (MFI)% (MFI)% (MFI)% (MFI)% (MFI)
 Control98.7(62083)40.2(671)56.0(2268)97.9(30985)10.6(377)35.1(438)44.0(775)35.1(367)
 mL4-3 + L1-7(N)99.1(60495)43.7(666)59.4(2670)99.1(35652)15.9(428)41.2(493)48.7(797)30.5(292)

The human ovarian cancer cell line OV17-1 (A), and human breast cancer cell line MDA-MB-231 (B) were treated with the Cmax of mL4-3 and L1-7(N) (16 and 10 μg/mL, respectively) or control (human IgG1-Fc at 26 μg/mL) for 3 days

Cells were then harvested and analyzed by flow cytometry for expression of surface markers reported to be involved in CTL lysis (HLA-A2, CEA, MUC-1, ICAM-1, calreticulin, Fas, Trail-R1 and Trail-R2). Data indicate percentage of positive cells; MFI is in parentheses. Gating was performed using isotype controls Bold values indicate marker upregulation of > 10 % in percentage or MFI compared to controls