Loss of α-tubulin acetylation is associated with TGF-β-induced epithelial-mesenchymal transition

Shuchen Gu, Yanjing Liu, Bowen Zhu, Ke Ding, Tso Pang Yao, Fenfang Chen, Lixing Zhan, Pinglong Xu, Marcelo Ehrlich, Tingbo Liang, Xia Lin, Xin Hua Feng*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The epithelial-to-mesenchymal transition (EMT) is a process by which differentiated epithelial cells reprogram gene expression, lose their junctions and polarity, reorganize their cytoskeleton, increase cell motility and assume a mesenchymal morphology. Despite the critical functions of the microtubule (MT) in cytoskeletal organization, how it participates in EMT induction and maintenance remains poorly understood. Here we report that acetylated α-tubulin, which plays an important role in microtubule (MT) stabilization and cell morphology, can serve as a novel regulator and marker of EMT. A high level of acetylated α-tubulin was correlated with epithelial morphology and it profoundly decreased during TGF-β-induced EMT. We found that TGF-β increased the activity of HDAC6, a major deacetylase of α-tubulin, without affecting its expression levels. Treatment with HDAC6 inhibitor tubacin or TGF-β type I receptor inhibitor SB431542 restored the level of acetylated α-tubulin and consequently blocked EMT. Our results demonstrate that acetylated α-tubulin can serve as a marker of EMT and that HDAC6 represents an important regulator during EMT process.

Original languageEnglish
Pages (from-to)5396-5405
Number of pages10
JournalJournal of Biological Chemistry
Issue number10
StatePublished - 4 Mar 2016


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