In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 1893-1893
Abstract:
Acetylation of α-tubulin has characterized as a key process for microtubule stabilization, and it can regulate cell spreading and modulate the dynamics of focal adhesion. 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. However, the physiological function of MEC-17 in cancer cells and its effect on MT acetylation during cell morphogenesis and migration has remained elusive. In the present study, our results showed that overexpression of MEC-17 induced increment of cell focal adhesion area, suppressed pseudopods formation in three-dimension collagen-embedded cultured environment and inhibited cancer cell migratory and invasive abilities. These changes were further proved to be caused by epithelial-mensenchymal transition (EMT) repression, cell polarity disruption caused by alteration of Golgi orientation and cdc42 activity and the decrease in the phosphorylation of extracellular signal regulatedkinase1/2 (Erk1/2). On the contrary, silencing of endogenous MEC-17 by specific shRNA accelerated the pseudopods formation and EMT process, which lead to facilitating the cell migration. Taken together, these results demonstrated that the important role of MEC-17 in the modulation of intrinsic cellular morphogenesis and migratory and invasive functions through regulation of EMT and polarization. (The study was supported by the following grants: MOST 103-2320-B-006-036-MY3 and MOST 105-2325-B-400-001 from the Ministry of Science and Technology of Taiwan, ROC) Citation Format: Cheng-Che Lee, Chi-Yen Chang, Chi-Min Lin, Jang-Yang Chang. Alpha-tubulin acetyltransferase, MEC-17, regulates cancer cell morphology and migration through epithelial-mesenchymal transition suppression and cell polarity disruption [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1893. doi:10.1158/1538-7445.AM2017-1893
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM2017-1893
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2017
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
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