Z-L Ma1, Y-P Chen, J-L Song, Y-Q Wang. 1. Department of Breast Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China. chenyanpingqd@sina.com.
Abstract
OBJECTIVE: CD24 is overexpressed in breast cancer, and patients with high CD24 expression was resistant to tamoxifen treatment. Furthermore, treatment with CD24 antibody 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 METHODS: 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 thiazolyl blue tetrazolium bromide (MTT), ELISA and terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) assays. The effects of CD24 knockdown on cell invasion and migration were determined using 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.
OBJECTIVE:CD24 is overexpressed in breast cancer, and patients with high CD24 expression was resistant to tamoxifen treatment. Furthermore, treatment with CD24 antibody 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 METHODS: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 thiazolyl blue tetrazolium bromide (MTT), ELISA and terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) assays. The effects of CD24 knockdown on cell invasion and migration were determined using 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 humanbreast cancer.
Authors: Jason E Duex; Charles Owens; Ana Chauca-Diaz; Garrett M Dancik; Lauren A Vanderlinden; Debashis Ghosh; Mariah Z Leivo; Donna E Hansel; Dan Theodorescu Journal: Cancer Res Date: 2017-07-03 Impact factor: 12.701
Authors: Euphemia Y Leung; Marjan E Askarian-Amiri; Debina Sarkar; Carole Ferraro-Peyret; Wayne R Joseph; Graeme J Finlay; Bruce C Baguley Journal: Front Oncol Date: 2017-09-04 Impact factor: 6.244