Erratum: CDK5 is essential for TGF-β1-induced epithelial-mesenchymal transition and breast cancer progression

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作者
Qian Liang
Lili Li
Jianchao Zhang
Yang Lei
Liping Wang
Dong-Xu Liu
Jingxin Feng
Pingfu Hou
Ruosi Yao
Yu Zhang
Baiqu Huang
Jun Lu
机构
[1] Northeast Normal University,The Key Laboratory of Molecular Epigenetics of Ministry of Education (MOE)
[2] The Institute of Genetics and Cytology,The Pathology Department
[3] Northeast Normal University,undefined
[4] the China-Japan Friendship Hospital of Jilin University,undefined
[5] The Liggins Institute,undefined
[6] the University of Auckland,undefined
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Epithelial-mesenchymal transition is a change of cellular plasticity critical for embryonic development and tumor metastasis. CDK5 is a proline-directed serine/threonine kinase playing important roles in cancer progression. Here we show that CDK5 is commonly overexpressed and significantly correlated with several poor prognostic parameters of breast cancer. We found that CDK5 participated in TGF-β1-induced EMT. In MCF10A, TGF-β1 upregulated the CDK5 and p35 expression, and CDK5 knockdown inhibited TGF-β1-induced EMT. CDK5 overexpression also exhibited a potential synergy in promoting TGF-β1-induced EMT. In mesenchymal breast cancer cells MDA-MB-231 and BT549, CDK5 knockdown suppressed cell motility and tumorigenesis. We further demonstrated that CDK5 modulated cancer cell migration and tumor formation by regulating the phosphorylation of FAK at Ser-732. Therefore, CDK5-FAK pathway, as a downstream step of TGF-β1 signaling, is essential for EMT and motility in breast cancer cells. This study implicates the potential value of CDK5 as a molecular marker for breast cancer.
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