Research Papers:

Ca2+/calmodulin-dependent protein kinase IIγ enhances stem-like traits and tumorigenicity of lung cancer cells

Shoujie Chai, Xia Xu, Yongfang Wang, You Zhou, Chenchen Zhang, Yiming Yang, Ying Yang, Haiyan Xu, Rongzhen Xu and Kai Wang _

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Oncotarget. 2015; 6:16069-16083. https://doi.org/10.18632/oncotarget.3866

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Shoujie Chai1,*, Xia Xu1,*, Yongfang Wang1, You Zhou1, Chenchen Zhang1, Yiming Yang1, Ying Yang1, Haiyan Xu1, Rongzhen Xu2 and Kai Wang1

1 Department of Respiratory Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

2 Department of Hematology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China

* These authors have contributed equally to this work

Correspondence to:

Kai Wang, email:

Keywords: CaMKIIγ, stem-like, tumorigenicity, lung cancer

Received: February 10, 2015 Accepted: March 31, 2015 Published: April 19, 2015


Highly tumorigenic stem-like cells, considered tumor-initiating cells (TICs), are the main cause of lung cancer initiation, relapse, and drug resistance. In this study, we identified that Ca2+/calmodulin-dependent protein kinase IIγ (CaMKIIγ) was aberrantly expressed in highly tumorigenic stem-like lung cancer cells, and was also correlated with poor prognosis in human lung cancer. Functionally, CaMKIIγ enhanced stem-like traits and the tumorigenicity of lung cancer cells in an Akt- and β-catenin-dependent manner. In addition, we found that CaMKIIγ upregulated Oct4 expression via Akt-mediated histone acetylation. Taken together, our findings reveal a critical role of CaMKIIγ in regulating the stemness and tumorigenicity of lung cancer cells and offer a promising therapeutic target for TICs.

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PII: 3866