Induction of epithelial-mesenchymal transition (EMT) by Beclin 1 knockdown via posttranscriptional upregulation of ZEB1 in thyroid cancer cells
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Si Li1,*, Hai-Yan Zhang2,*, Zhen-Xian Du3, Chao Li1, Ming-Xin An1, Zhi-Hong Zong1, Bao-Qin Liu1, Hua-Qin Wang1
1Department of Biochemistry and Molecular Biology, China Medical University, Shenyang 110001, China
2Department of Geriatrics, the 1st Affiliated Hospital, China Medical University, Shenyang 110001, China
3Department of Endocrinology and Metabolism, the 1st Affiliated Hospital, China Medical University, Shenyang 110001, China
*These authors contributed equally to this work
Hua-Qin Wang, email: email@example.com
Keywords: Beclin1, EMT, invasion, thyroid cancer
Received: May 02, 2016 Accepted: September 02, 2016 Published: September 23, 2016
Beclin 1 has emerged as a haploinsufficient tumor suppression gene in a variety of human carcinomas. In order to clarify the role of Beclin 1 in thyroid cancer, Beclin 1 was knockdown in thyroid cancer cell lines. The current study demonstrated that knockdown of Beclin 1 resulted in morphological and molecular changes of thyroid cancer cells consistent with epithelial-mesenchymal transition (EMT), a morphogenetic procedure during which cells lose their epithelial characteristics and acquire mesenchymal properties concomitantly with gene expression reprogramming. In addition, the current study presented evidence demonstrating that Beclin 1 knockdown triggered this prometastatic process via stabilization of the EMT inducer ZEB1 mRNA through upregulation of AU-binding factor 1 (AUF1), which is recruited to the 3’-untranslated region (UTR) of the ZEB1 mRNA and decreases its degradation. We also found a negative correlation of Beclin 1 with AUF1 or ZEB1 in thyroid cancer tissues. These results indicated that at least some tumor suppressor functions of Beclin 1 were mediated through posttranscriptional regulation of ZEB1 via AUF1 in thyroid cancers.
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