Effects of Wnt proteins on cell proliferation and apoptosis in HEK293 cells

Authors

  • Liwei Jia,

    1. State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, PR China
    2. Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 100039, PR China
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  • Chenglin Miao,

    1. State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, PR China
    2. Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 100039, PR China
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  • Yujing Cao,

    1. State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, PR China
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  • En Kui Duan

    Corresponding author
    1. State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Datun Road, Chaoyang District, Beijing 100101, PR China
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Corresponding author. Tel.: +86 10 64807186; fax: +86 10 64807099. duane@ioz.ac.cn

Abstract

Wnt proteins and Wnt signalings have been implicated in a variety of development and cell processes, while aberrant activation of Wnt signaling is linked to a range of cancers in many tissues. In this study, we used the HEK293 cell line to investigate the effects of Wnt3a and Wnt5a on proliferation and apoptosis in a serum starvation culture. After Wnt3a and Wnt5a proteins were expressed, they both promoted the proliferation of HEK293 cells under serum starvation. After 48 h of serum starvation, both Wnt3a and Wnt5a inhibited serum starvation-induced apoptosis of HEK293 cells and continued up to 96 h. We demonstrated that Wnt3a and Wnt5a can promote proliferation of HEK293 cells and inhibit serum starvation-induced apoptosis, which implies that Wnt3a and Wnt5a can maintain the survival of HEK293 cells under stress, and also provide a novel insight into the role of Wnt3a and Wnt5a and their related signalings in carcinogenesis.

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