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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: We found that expression of CD24 was increased by stable overexpression of HER2.Knockdown of CD24 also suppressed the phosphorylation of Akt, which functions downstream of HER2 and PI3K to promote cell survival.Our results thus indicate that CD24 supports both the expression of HER2 and the consequent activation of PI3K-Akt signaling.

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: We found that expression of CD24 was increased by stable overexpression of HER2.Knockdown of CD24 also suppressed the phosphorylation of Akt, which functions downstream of HER2 and PI3K to promote cell survival.Our results thus indicate that CD24 supports both the expression of HER2 and the consequent activation of PI3K-Akt signaling.

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