Abstract
Objective To establish interleukin -11 receptor α (IL-11Rα)-based 131I-CGRRAGGSC by chloramines-T method, and explore the inhibitory effects of 131I-CGRRAGGSC on human breast cancer cells overexpressing IL-11Rα. Methods The tyrosine modified CGRRAGGSC protein was labeled with 131I by chloramines-T method. Methyl thiazol tetrazolium (MTT), Transwell and wound-healing assay were used to detect the effects of 131I-CGRRAGGSC on the migration and proliferation of human breast cancer cells. Western blotting was used to detect the protein expression of IL-11Rα, phosphorylated signal transducer and activators of transcription 3 (p-STAT3) and signal transducer and activators of transcription 3 (STAT3) in breast cancer cells after treatment with 0, 2.775 and 5.550 MBq/ml 131I-CGRRAGGSC. Results 131I-CGRRAGGSC was radiolabeled successfully and radiochemical purity after purification was over 95%. The inhibition ratio of breast cancer cells (MDA-MB-231 and MCF-7) was (21.46±1.08)%, (37.95±2.59)%, (49.18±0.77)%, (60.34±0.19)% (F=389.4, P=0.000) and (27.59±2.15)%, (41.67±0.92)%, (54.53±1.07)%, (64.84±1.69)% (F=328.6, P=0.000) after 131I-CGRRAGGSC treatment (4.625, 9.250, 18.500 and 37.000 MBq/ml, respectively). Transwell demonstrated that the migration ratios of 2.775, 5.55 MBq/ml 131I-CGRRAGGSC were (32.05±4.44)%, (45.92±2.55)% (t=4.688, P=0.009) for MDA-MB-231 cells and (21.99±1.18)%, (39.45±1.36)% (t=16.760, P=0.000) for MCF-7 cells, respectively. Wound-healing assay also suggested that 131I-CGRRAGGSC inhibited MDA-MB-231 cells, but not MCF-7 cells. The cellular IL-11Rα and p-STAT3 levels were decreased in a dose-dependent manner whereas the STAT3 level had no significant change in 131I-CGRRAGGSC-treated breast cancer cells after 24 h in compared to those in the control cells. Conclusion 131I-CGRRAGGSC could inhibit the migration and proliferation of human breast cancer cells by down-regulating the IL-11Rα to inhibit STAT3 activation. Key words: Breast cancer; Radiolabeling; Migration; 131I
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