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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 suppresses Akt phosphorylation in human epidermal growth factor receptor 2 (HER2)-expressing cells. The abundance of total or phosphorylated forms of HER2, Akt, Erk1/2, EGFR and HER3 was examined by immunoblot analysis in BT-474, HCC202 and HCC1569 cells (a) as well as in 231-Luc, HER2-60 and HER2-90 cells (b) that had been transfected with control (GAPD) or CD24 siRNAs for 48 h.
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fig06: Knockdown of CD24 suppresses Akt phosphorylation in human epidermal growth factor receptor 2 (HER2)-expressing cells. The abundance of total or phosphorylated forms of HER2, Akt, Erk1/2, EGFR and HER3 was examined by immunoblot analysis in BT-474, HCC202 and HCC1569 cells (a) as well as in 231-Luc, HER2-60 and HER2-90 cells (b) that had been transfected with control (GAPD) or CD24 siRNAs for 48 h.

Mentions: Western blot analysis also showed that the knockdown of CD24 by siRNA decreased the expression and the phosphorylation of HER2 in the HER2-positive cell lines, BT-474, HCC202, and HCC1569 (Fig. 6a). However, in 231-Luc derived cells, HER2-60 and HER2-90, the exogenous HER2 expression driven by the cytomegalovirus (CMV) promoter was not affected by siRNA-mediated CD24 depletion (Fig. 6b).


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 suppresses Akt phosphorylation in human epidermal growth factor receptor 2 (HER2)-expressing cells. The abundance of total or phosphorylated forms of HER2, Akt, Erk1/2, EGFR and HER3 was examined by immunoblot analysis in BT-474, HCC202 and HCC1569 cells (a) as well as in 231-Luc, HER2-60 and HER2-90 cells (b) that had been transfected with control (GAPD) or CD24 siRNAs for 48 h.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig06: Knockdown of CD24 suppresses Akt phosphorylation in human epidermal growth factor receptor 2 (HER2)-expressing cells. The abundance of total or phosphorylated forms of HER2, Akt, Erk1/2, EGFR and HER3 was examined by immunoblot analysis in BT-474, HCC202 and HCC1569 cells (a) as well as in 231-Luc, HER2-60 and HER2-90 cells (b) that had been transfected with control (GAPD) or CD24 siRNAs for 48 h.
Mentions: Western blot analysis also showed that the knockdown of CD24 by siRNA decreased the expression and the phosphorylation of HER2 in the HER2-positive cell lines, BT-474, HCC202, and HCC1569 (Fig. 6a). However, in 231-Luc derived cells, HER2-60 and HER2-90, the exogenous HER2 expression driven by the cytomegalovirus (CMV) promoter was not affected by siRNA-mediated CD24 depletion (Fig. 6b).

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