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Molecular Cancer Research
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Cell Cycle, Cell Death, and Senescence

Protein Kinase Casein Kinase 2–Mediated Upregulation of N-Cadherin Confers Anoikis Resistance on Esophageal Carcinoma Cells

Hyeonseok Ko, Seongrak Kim, Cheng-Hao Jin, Eunjung Lee, Sunyoung Ham, Jong In Yook and Kunhong Kim
Hyeonseok Ko
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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Seongrak Kim
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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Cheng-Hao Jin
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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Eunjung Lee
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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Sunyoung Ham
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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Jong In Yook
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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Kunhong Kim
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
Authors' Affiliations: 1Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine; 2Brain Korea 21 Project for Medical Science of Yonsei University; 3Department of Oral Pathology; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea
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DOI: 10.1158/1541-7786.MCR-12-0261 Published August 2012
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    Figure 1.

    PKCK2 activity and anoikis. A, TE2, TE3, HCE4, or HCE7 cells were cultured on the poly-HEMA-coated tissue culture plates for the indicated times and tested for viability with the SRB assay. The data are expressed as mean ± SD for triplicates. B, TE2 and HCE4 cells were plated on poly-HEMA-coated tissue culture plate (Poly-HEMA+) and photographed using phase contrast microscopy 16 hours after plating. C, Western blot analysis was conducted to confirm apoptosis using cell lysates for the indicated time points.

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    Figure 2.

    Cadherin expression and anoikis. A, Western blot analysis of epithelial or mesenchymal markers and PKB/Akt activation. B, N-cadherin downregulation, PKB/Akt inactivation, and anoikis. HCE4 cells were transfected with either a scrambled siRNA (Sc) or N-cadherin siRNA (N) for 48 hours. The cells were then cultured on poly-HEMA-coated plates for 48 hours. Cell viability assay (left) and Western blot analysis (right) were carried out. The data are expressed as mean ± SD for triplicates.

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    Figure 3.

    E-to N-cadherin switching and anoikis resistance. A, TE2 cells were transduced with lentivirus-expressing HA-tagged PKCK2 α catalytic subunit. Western blot analysis and in vitro kinase assay for intracellular PKCK2 activity were conducted. 32P-GST-CS (GST-tagged recombinant CK2 Substrate) represents phosphorylated GST-CS and GST-CS represents Coomassie blue stained input GST-CS. B, TE2-GFP and TE2-CK2α cells were cultured on poly-HEMA-coated plates for 48 hours. Western blot analysis (top) and cell viability assay (bottom) were conducted. The data are expressed as mean ± SD for triplicates. C, TE2-CK2α cells were transfected with either a scrambled siRNA (Sc) or N-cadherin siRNA (N) for 48 hours. The cells were then cultured on poly-HEMA-coated plates for 48 hours. Western blot analysis (top) and cell viability assay (bottom) were conducted. The data are expressed as mean ± SD for triplicates.

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    Figure 4.

    N-to E-cadherin switching and anoikis. A, HCE4 cells were stably transfected with shRNA against PKCK2 α catalytic subunit and treated with puromycin for selection. Western blot analysis and in vitro kinase assay for intracellular PKCK2 activity were conducted. B, HCE4-VC (Vector control) and HCE4-CKD (CK2 α knockdown) cells were cultured on poly-HEMA-coated plates for 48 hours. Western blot analysis (top) and cell viability assay (bottom) were conducted. The data are expressed as mean ± SD for triplicates.

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    Figure 5.

    N-cadherin expression and invasiveness. A, in vitro invasiveness of TE2, TE3, HCE4, and HCE7 cells were measured using a Cell Invasion Assay Kit. B, in vitro invasiveness of TE2-GFP and TE2-CK2α cells. C, in vitro invasiveness of HCE4 cells that were transfected with either a scrambled siRNA (Sc) or N-cadherin siRNA (N) for 48 hours. The data are expressed as mean ± SD for triplicates.

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    • Supplementary Figure 1 - PDF file - 71K, Western blot analysis for type of cadherin expressed in TE2, TE3, HCE4, and HCE7 (A) and for epithelial or mesenchymal markers and PKB/Akt activation in TE3 and HCE7 cells (B)
    • Supplementary Figure 2 - PDF file - 59K, PKCK2 activity dependent stabilization of exogenous Snail. A, MCF-7 cells that have low PKCK2 activity were co-transfected with Flag tagged Snail expression vector along either with empty vector or with Myc tagged PKCK2� expression vector. B, HCE4 cells were transfected with Flag-Snail and then were treated or un-treated with TBB, a pharmacologic inhibitor of PKCK2. C, PKCK2 activity was measured for each condition. S92 represents a vector expressing wild type snail, S92A (serine 92 replaced with alanine) mutant represents a vector expressing non-phosphorylatable form of snail, and S92E (serine 92 replaced with glutamic acid) represents a vector expressing mutant snail to mimic constitutive phosphorylation
    • Supplementary Figure 3 - PDF file - 79K, Expression level of molecules involved in E-cadherin down-regulation. Western blot analysis was performed using total cell lysates (A) or lysates from cytoplasmic or nuclear fraction (B). The indicated Abs were used. RT-PCR was performed to examine mRNA expression level of Axin2 in TE2 and HCE4 cells and GAPDH was used as an internal control
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Molecular Cancer Research: 10 (8)
August 2012
Volume 10, Issue 8
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Protein Kinase Casein Kinase 2–Mediated Upregulation of N-Cadherin Confers Anoikis Resistance on Esophageal Carcinoma Cells
Hyeonseok Ko, Seongrak Kim, Cheng-Hao Jin, Eunjung Lee, Sunyoung Ham, Jong In Yook and Kunhong Kim
Mol Cancer Res August 1 2012 (10) (8) 1032-1038; DOI: 10.1158/1541-7786.MCR-12-0261

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Protein Kinase Casein Kinase 2–Mediated Upregulation of N-Cadherin Confers Anoikis Resistance on Esophageal Carcinoma Cells
Hyeonseok Ko, Seongrak Kim, Cheng-Hao Jin, Eunjung Lee, Sunyoung Ham, Jong In Yook and Kunhong Kim
Mol Cancer Res August 1 2012 (10) (8) 1032-1038; DOI: 10.1158/1541-7786.MCR-12-0261
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