Knockdown of CD24 inhibits proliferation, invasion and sensitizes breast cancer MCF-7 cells to tamoxifen in vitro

Z.-L Ma, Y.-P Chen, J.-L Song, Y.-Q Wang
unpublished
OBJECTIVE: CD24 is overex-pressed in breast cancer, and patients with high CD24 expression was resistant to tamoxifen treatment. Furthermore, treatment with CD24 an-tibody to inhibit CD24 expression could induce apoptosis and inhibits migration in breast cancer cells in vitro. In this study, we investigated the anti-tumor efficacy of CD24 knockdown using siRNA targeting CD24 on proliferation, invasion and sensitivity to tamoxifen (TAM) of breast cancer MCF-7 cells in vitro. MATERIALS AND
more » ... : CD24 siRNA vector (CD24-siRNA) and empty plasmid vector (EP) were transiently transfected into the breast cancer MCF-7 cells and the knockdown efficacy was assessed by Western blot analysis. The effects of CD24 knockdown on cell viability , apoptosis and sensitivity to TAM in MCF-7 cells were determined using methyl thi-azolyl blue tetrazolium bromide (MTT), ELISA and terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) assays. The effects of CD24 knockdown on cell invasion a n d m i g r a t i o n w e r e d e t e r m i n e d u s i n g chemoinvasion assay and wound scratch assay , respectively. RESULTS: Transfection of CD24-siRNA effectively down-regulated CD24 expression in MCF-7 cells in vitro. CD24 suppressed showed significantly decreased proliferation, invasion and increased apoptosis as well as increased sensitivity to TAM in vitro in MCF-7 cells. CONCLUSIONS: Knockdown of CD24 expression by CD24-siRNA significantly inhibited invasion and cell viability, and induced apoptosis and increased sensitivity of MCF-7 cells to TAM, indicating that knockdown of CD24 by siRNA might be a potential therapeutic approach against human breast cancer.
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