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Research ArticlePROCEEDINGS OF THE CHINA –UNITED KINGDOM CANCER (CUKC) CONFERENCE 2015 (Cardiff, Wales, UK)

Targeting of Receptor Activator of Nuclear Kappa B (RANK) in PC-3 Cells Increases Cell Proliferation and Matrix Adhesion In Vitro

SIONED OWEN, ANDREW J. SANDERS, MALCOLM D. MASON and WEN G. JIANG
Anticancer Research March 2016, 36 (3) 1127-1134;
SIONED OWEN
1Cardiff China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff, U.K.
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  • For correspondence: OwenS15@cf.ac.uk
ANDREW J. SANDERS
1Cardiff China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff, U.K.
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MALCOLM D. MASON
2Oncology and Palliative Medicine, Velindre Hospital, Cardiff, U.K.
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WEN G. JIANG
1Cardiff China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff, U.K.
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    Figure 1.

    Verification of ribozyme transgene knockdown of Receptor Activator of Nuclear Kappa B (RANK) in PC-3 cells. Reduced RANK expression (PC-3RANKKD) was confirmed in PC-3 cells at the transcript level using conventional polymerase chain reaction (A) and quantitative polymerase chain reaction (B) compared to the pEF6 control cell line. Western blotting was used to confirm successful RANK knockdown (C) normalized against glyceraldehyde 3-phosphate dehydrogenase (GAPDH). **p≤0.01. Data are the mean of n=4, error bars show SEM.

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    Figure 2.

    Impact of Receptor Activator of Nuclear Kappa B (RANK) knockdown on PC-3 cell proliferation. Suppression of RANK expression in PC-3 cells (PC-3RANKKD) resulted in a significant increase in PC-3 cell proliferation after 3 (A) and 5 (B) days compared to control cells. When control PC-3 (C) and PC-3RANKKD (D) cells were treated with 40 ng/ml hepatocyte growth factor (HGF) for 3 days, no significant increase in PC-3 cell proliferation was seen. However, after 5 days' incubation, control cells treated with HGF showed significantly increased cell proliferation (E), a trend that was not seen in RANK-suppressed cells when compared to untreated RANK-suppressed control cells (F). **p≤0.01, ***p≤0.001. Data are the mean of n=3, error bars show SEM.

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    Figure 3.

    Impact of Receptor Activator of Nuclear Kappa B (RANK) knockdown on PC-3 cell-matrix adhesion. Suppression of RANK expression in PC-3 cells (PC-3RANKKD) resulted in a significant increase in cell-matrix adhesion (A) compared to control cells. When control (B) and PC-3RANKKD (C) cells were treated with hepatocyte growth factor (HGF), no significant changes in cell-matrix adhesion were seen. *p≤0.05. Data are the mean of n=3, error bars show SEM.

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    Figure 4.

    Impact of Receptor Activator of Nuclear Kappa B (RANK) knockdown on PC-3 cell motility. Suppression of RANK expression in PC-3 cells (PC-3RANKKD) did not affect cell motility (A) compared to the control cells. When control (B) and PC-3RANKKD cells (C) were treated with hepatocyte growth factor (HGF), no significant changes in cell motility were seen. Data are the mean of n=3, error bars show SEM.

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    Figure 5.

    Impact of Receptor Activator of Nuclear Kappa B (RANK) knockdown on PC-3 cell invasion. Suppression of RANK expression in PC-3 cells did not affect cell invasion (A) compared to control cells. When control cells (B) were treated with hepatocyte growth factor (HGF), cell invasion significantly increased compared to the untreated control, a trend which was not seen in RANK-suppressed PC-3 cells (C). *p≤0.05. Data are the mean of n=3, error bars show SEM.

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Anticancer Research: 36 (3)
Anticancer Research
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March 2016
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Targeting of Receptor Activator of Nuclear Kappa B (RANK) in PC-3 Cells Increases Cell Proliferation and Matrix Adhesion In Vitro
SIONED OWEN, ANDREW J. SANDERS, MALCOLM D. MASON, WEN G. JIANG
Anticancer Research Mar 2016, 36 (3) 1127-1134;

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Targeting of Receptor Activator of Nuclear Kappa B (RANK) in PC-3 Cells Increases Cell Proliferation and Matrix Adhesion In Vitro
SIONED OWEN, ANDREW J. SANDERS, MALCOLM D. MASON, WEN G. JIANG
Anticancer Research Mar 2016, 36 (3) 1127-1134;
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