CD24 cross-linking induces apoptosis in, and inhibits migration of, MCF-7 breast cancer cells

Jong Bin Kim, Eunyoung Ko, Wonshik Han, Jeong Eon Lee, Kyung Min Lee, Incheol Shin, Sangmin Kim, Jong Won Lee, Jihyoung Cho, Ji Yeon Bae, Hyeon Gun Jee, Dong Young Noh

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Abstract

Background: The biological effects of CD24 (FL-80) cross-linking on breast cancer cells have not yet been established. We examined the impact of CD24 cross-linking on human breast cancer cell line MCF-7. Methods: MCF-7 and MDA-MB-231 cells were treated with anti-rabbit polyclonal IgG or anti-human CD24 rabbit polyclonal antibodies to induce cross-linking, and then growth was studied. Changes in cell characteristics such as cell cycle modulation, cell death, survival in three-dimensional cultures, adhesion, and migration ability were assayed after CD24 cross-linking in MCF-7. Results: Expression of CD24 was analyzed by flow cytometry in MDA-MB-231 and MCF-7 cells where 2% and 66% expression frequencies were observed, respectively. CD24 cross-linking resulted in time-dependent proliferation reduction in MCF-7 cells, but no reduction in MDA-MB-231 cells. MCF-7 cell survival was reduced by 15% in three-dimensional culture after CD24 cross-linking. Increased MCF-7 cell apoptosis was observed after CD24 cross-linking, but no cell cycle arrest was observed in that condition. The migration capacity of MCF-7 cells was diminished by 30% after CD24 cross-linking. Conclusion: Our results showed that CD24 cross-linking induced apoptosis and inhibited migration in MCF-7 breast cancer cells. We conclude that CD24 may be considered as a novel therapeutic target for breast cancer.

Original languageEnglish
Article number118
JournalBMC Cancer
Volume8
DOIs
StatePublished - 24 Apr 2008

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Kim, J. B., Ko, E., Han, W., Lee, J. E., Lee, K. M., Shin, I., Kim, S., Lee, J. W., Cho, J., Bae, J. Y., Jee, H. G., & Noh, D. Y. (2008). CD24 cross-linking induces apoptosis in, and inhibits migration of, MCF-7 breast cancer cells. BMC Cancer, 8, [118]. https://doi.org/10.1186/1471-2407-8-118