ArticleScientific reports2018
Alpha-tubulin acetyltransferase/MEC-17 regulates cancer cell migration and invasion through epithelial-mesenchymal transition suppression and cell polarity disruption.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Phospho-JNK agonists show promising effects for the treatment of hepatocellular carcinoma.iScience · 2026Article
- α-tubulin N-acetyltransferase 1 regulates NCOA4-mediated ferritinophagy and protects cancer cells from ferroptosis.Cellular & molecular biology letters · 2026Article
- OptoTAT reveals microtubule acetylation as a rapid trigger for GEF-H1-mediated cell migration.The Journal of cell biology · 2026Article
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Tubulin acetyltransferases access and modify the microtubule luminal K40 residue through anchors in taxane-binding pockets.Nature structural & molecular biology · 2025Article
- Luminal acetylation of microtubules is not essential forMicrobial cell (Graz, Austria) · 2025Article
- Tubulin Acetylation: A Critical Regulator of Microtubule Function.Results and problems in cell differentiation · 2025Review
- Optogenetically Induced Microtubule Acetylation Unveils the Molecular Dynamics of Actin-Microtubule Crosstalk in Directed Cell Migration.bioRxiv : the preprint server for biology · 2024Article
- The α-tubulin acetyltransferase ATAT1: structure, cellular functions, and its emerging role in human diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Role of Exosomes in Epithelial-Mesenchymal Transition.ACS applied bio materials · 2024Review
- Regulatory roles of NAT10 in airway epithelial cell function and metabolism in pathological conditions.Cell biology and toxicology · 2023Article
- Review
- Non-catalytic allostery in α-TAT1 by a phospho-switch drives dynamic microtubule acetylation.The Journal of cell biology · 2022Article
- MPP7 as a Novel Biomarker of Esophageal Cancer: MPP7 Knockdown Inhibits Esophageal Cancer Cell Migration and Invasion.Life (Basel, Switzerland) · 2022Article
- HDAC8-Selective Inhibition by PCI-34051 Enhances the Anticancer Effects of ACY-241 in Ovarian Cancer Cells.International journal of molecular sciences · 2022Article
- Epithelial-Mesenchymal Transition-Mediated Tumor Therapeutic Resistance.Molecules (Basel, Switzerland) · 2022Review
- LukS-PV inhibits hepatocellular carcinoma cells migration by downregulating HDAC6 expression.BMC cancer · 2022Article
- Perphenazine and prochlorperazine decrease glioblastoma U-87 MG cell migration and invasion: Analysis of the ABCB1 and ABCG2 transporters, E-cadherin, α-tubulin and integrins (α3, α5, and β1) levels.Oncology letters · 2022Article
- Review
- Downregulation of miR‑29b‑3p promotes α‑tubulin deacetylation by targeting the interaction of matrix metalloproteinase‑9 with integrin β1 in nasal polyps.International journal of molecular medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
MEC-17, a newly identified alpha-tubulin-N-acetyltransferase 1, serves as the major α-tubulin acetyltransferase to promote α-tubulin acetylation in vitro and in vivo. Alteration of α-tubulin acetylation may be involved in morphology regulation, cell migration, and tumour metastasis. However, MEC-17's role in cell physiology and its effect on epithelial-mesenchymal transition (EMT) and cell polarity remain elusive. In the present study, we characterized the overexpressed or downregulated cell models through gene targeting as MEC-17 gain- or loss-of-function. Overexpression of MEC-17 enhanced the cell spreading area, suppressed pseudopods formation in a three-dimensional (3D) culture system, and inhibited cancer cell migratory and invasive ability and tumour metastasis by orthotopic lung cancer animal model. Furthermore, morphological change and migration inhibition of cancer cells were accompanied by EMT repression, Golgi reorientation, and polarity disruption caused by alteration of cdc42 activity via a decrease in Rho-GAP, ARHGAP21. By contrast, a reduction in endogenous MEC-17 accelerated the pseudopods formation and EMT, and facilitated cell migration and invasion. These results demonstrated the crucial role of MEC-17 in the modulation of intrinsic cell morphogenesis, migration, and invasive function through regulation of EMT and cell polarity.
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