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Inhibition of atypical protein kinase Cι induces apoptosis through autophagic degradation of β-catenin in esophageal cancer cells

Authors

  • Bo-Shi Wang,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Yang Yang,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
    2. Department of Histology and Embryology, Anhui Medical University, Hefei, China
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  • Hai-Zhen Lu,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Li Shang,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Yu Zhang,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Jia-Jie Hao,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Zhi-Zhou Shi,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Xiao-Min Wang,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Yi-Zhen Liu,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Qi-Min Zhan,

    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
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  • Xue-Mei Jia,

    Corresponding author
    1. Department of Histology and Embryology, Anhui Medical University, Hefei, China
    • State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), PUMC/CAMS, 17 Panjiayuan Nanli, Chaoyang District, Beijing 100021, China.

      Department of Histology and Embryology, Anhui Medical University, 81 Meishan Road, Hefei 230032, China.

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  • Ming-Rong Wang

    Corresponding author
    1. State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China
    • State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), PUMC/CAMS, 17 Panjiayuan Nanli, Chaoyang District, Beijing 100021, China.

      Department of Histology and Embryology, Anhui Medical University, 81 Meishan Road, Hefei 230032, China.

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  • The authors declare no conflict of interest.

Abstract

Atypical protein kinase Cι (PKCι) has been identified as an oncoprotein in esophageal squamous cell carcinomas. However, the mechanisms underlying the role of PKCι in this disease remain unclear. In the present work, we found that inhibition of PKCι expression by RNAi induced apoptosis via the down-regulation of β-catenin in esophageal cancer cells. Furthermore, we found that PKCι regulated β-catenin in an autophagy dependent way. Since down-regulation of β-catenin induced by knockdown of PKCι could be rescued by autophagy inhibition; knockdown of PKCι activated autophagy and promoted the recruitment of β-catenin into autophagosome. These results suggested that PKCι positively regulated β-catenin through negatively regulated autophagy and depletion of PKCι promoted apoptosis via autophagic degradation of β-catenin in esophageal cancer cells. These data provide new insights into PKCι signaling in human cancer. © 2013 Wiley Periodicals, Inc.

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