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Expression of CD24 is associated with HER2 expression and supports HER2-Akt signaling in HER2-positive breast cancer cells.

Hosonaga M, Arima Y, Sugihara E, Kohno N, Saya H - Cancer Sci. (2014)

Bottom Line: However, resistance to HER2-targeted therapy remains a major clinical problem.HER2-positive breast tumors are predominantly positive for CD24, suggesting that the expression of the two molecules is related.Flow cytometry thus revealed that the percentage of CD24-positive cells was markedly higher in the HER2-positive fraction than in the HER2-negative fraction.

View Article: PubMed Central - PubMed

Affiliation: Division of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, Tokyo, Japan; Department of Breast Oncology, Tokyo Medical University, Tokyo, Japan.

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Knockdown of CD24 downregulates human epidermal growth factor receptor 2 (HER2) expression in BT-474 cells. (a) Quantitative RT-PCR analysis of CD24 and HER2 mRNA in cells transfected with CD24, HER2 or control (GAPD) siRNA, as indicated, for 48 h. Data are normalized by the amount of HPRT1 mRNA, expressed relative to the corresponding normalized value for cells transfected with GAPDsi, and are presented as means ± SD for triplicate experiments. ***P < 0.001 (Student's t test). (b) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with CD24 or control siRNA. (c) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with HER2 or control siRNA.
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fig05: Knockdown of CD24 downregulates human epidermal growth factor receptor 2 (HER2) expression in BT-474 cells. (a) Quantitative RT-PCR analysis of CD24 and HER2 mRNA in cells transfected with CD24, HER2 or control (GAPD) siRNA, as indicated, for 48 h. Data are normalized by the amount of HPRT1 mRNA, expressed relative to the corresponding normalized value for cells transfected with GAPDsi, and are presented as means ± SD for triplicate experiments. ***P < 0.001 (Student's t test). (b) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with CD24 or control siRNA. (c) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with HER2 or control siRNA.

Mentions: We examined whether CD24 might affect HER2 expression with the use of RNA interference in the HER2-positive cell line BT-474. The abundance of CD24 and HER2 mRNA was significantly reduced by transfection of the cells with corresponding targeted siRNA (Fig. 5a). Flow cytometry analysis revealed that the percentage of CD24-expressing cells was also markedly reduced by knockdown of CD24 (from 98.9% for cells transfected with a control siRNA to 56.2%). The HER2-negative faction was increased by transfection with the CD24 siRNA (from 71.3% to 59.8%) (Fig. 5b). In contrast, knockdown of HER2 did not affect the proportion of cells expressing CD24 (98.9% for the control siRNA versus 98.1% for the HER2 siRNA) (Fig. 5c). These results imply that CD24 plays a role in maintenance of HER2-positive cells.


Expression of CD24 is associated with HER2 expression and supports HER2-Akt signaling in HER2-positive breast cancer cells.

Hosonaga M, Arima Y, Sugihara E, Kohno N, Saya H - Cancer Sci. (2014)

Knockdown of CD24 downregulates human epidermal growth factor receptor 2 (HER2) expression in BT-474 cells. (a) Quantitative RT-PCR analysis of CD24 and HER2 mRNA in cells transfected with CD24, HER2 or control (GAPD) siRNA, as indicated, for 48 h. Data are normalized by the amount of HPRT1 mRNA, expressed relative to the corresponding normalized value for cells transfected with GAPDsi, and are presented as means ± SD for triplicate experiments. ***P < 0.001 (Student's t test). (b) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with CD24 or control siRNA. (c) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with HER2 or control siRNA.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4317915&req=5

fig05: Knockdown of CD24 downregulates human epidermal growth factor receptor 2 (HER2) expression in BT-474 cells. (a) Quantitative RT-PCR analysis of CD24 and HER2 mRNA in cells transfected with CD24, HER2 or control (GAPD) siRNA, as indicated, for 48 h. Data are normalized by the amount of HPRT1 mRNA, expressed relative to the corresponding normalized value for cells transfected with GAPDsi, and are presented as means ± SD for triplicate experiments. ***P < 0.001 (Student's t test). (b) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with CD24 or control siRNA. (c) Flow cytometric analysis of CD24, CD44 and HER2 expression in cells transfected with HER2 or control siRNA.
Mentions: We examined whether CD24 might affect HER2 expression with the use of RNA interference in the HER2-positive cell line BT-474. The abundance of CD24 and HER2 mRNA was significantly reduced by transfection of the cells with corresponding targeted siRNA (Fig. 5a). Flow cytometry analysis revealed that the percentage of CD24-expressing cells was also markedly reduced by knockdown of CD24 (from 98.9% for cells transfected with a control siRNA to 56.2%). The HER2-negative faction was increased by transfection with the CD24 siRNA (from 71.3% to 59.8%) (Fig. 5b). In contrast, knockdown of HER2 did not affect the proportion of cells expressing CD24 (98.9% for the control siRNA versus 98.1% for the HER2 siRNA) (Fig. 5c). These results imply that CD24 plays a role in maintenance of HER2-positive cells.

Bottom Line: However, resistance to HER2-targeted therapy remains a major clinical problem.HER2-positive breast tumors are predominantly positive for CD24, suggesting that the expression of the two molecules is related.Flow cytometry thus revealed that the percentage of CD24-positive cells was markedly higher in the HER2-positive fraction than in the HER2-negative fraction.

View Article: PubMed Central - PubMed

Affiliation: Division of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, Tokyo, Japan; Department of Breast Oncology, Tokyo Medical University, Tokyo, Japan.

Show MeSH
Related in: MedlinePlus