Loukil A, Cheung CT, Bendris N, Lemmers B, Peter M, Blanchard JM. Cyclin A2: At the crossroads of cell cycle and cell invasion. World J Biol Chem 2015; 6(4): 346-350 [PMID: 26629317 DOI: 10.4331/wjbc.v6.i4.346]
Corresponding Author of This Article
Jean Marie Blanchard, PhD, Institut de Génétique Moléculaire de Montpellier, CNRS, 1919 route de Mende, 34293 Montpellier, France. jean-marie.blanchard@igmm.cnrs.fr
Research Domain of This Article
Biochemical Research Methods
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Biol Chem. Nov 26, 2015; 6(4): 346-350 Published online Nov 26, 2015. doi: 10.4331/wjbc.v6.i4.346
Cyclin A2: At the crossroads of cell cycle and cell invasion
Abdelhalim Loukil, Caroline T Cheung, Nawal Bendris, Bénédicte Lemmers, Marion Peter, Jean Marie Blanchard
Abdelhalim Loukil, Caroline T Cheung, Nawal Bendris, Bénédicte Lemmers, Marion Peter, Jean Marie Blanchard, Institut de Génétique Moléculaire de Montpellier, CNRS, 34293 Montpellier, France
Abdelhalim Loukil, Caroline T Cheung, Nawal Bendris, Bénédicte Lemmers, Marion Peter, Jean Marie Blanchard, Université Montpellier, 34095 Montpellier, France
Abdelhalim Loukil, Department of Developmental and Cell Biology, University of California Irvine, Irvine, CA 92697, United States
Nawal Bendris, Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75235, United States
Author contributions: All the authors contributed equally to this work; Blanchard JM contributed to writing the paper.
Supported by Agence Nationale de la Recherche (08-BLAN-0037-02), Fondation ARC pour la Recherche sur le Cancer, and Gefluc; CNRS/Région Languedoc-Roussillon and Fondation pour la Recherche Médicale (Loukil A); the French Ministry of Education and Research and Fondation pour la Recherche Médicale (Bendris N); and the Canadian Institutes of Health Research, La Ligue Contre le Cancer and the Fondation de France (Cheung CT).
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Jean Marie Blanchard, PhD, Institut de Génétique Moléculaire de Montpellier, CNRS, 1919 route de Mende, 34293 Montpellier, France. jean-marie.blanchard@igmm.cnrs.fr
Telephone: +33-4-34359650 Fax: +33-4-34359634
Received: April 14, 2015 Peer-review started: April 14, 2015 First decision: May 13, 2015 Revised: September 18, 2015 Accepted: October 12, 2015 Article in press: October 13, 2015 Published online: November 26, 2015 Processing time: 222 Days and 16.6 Hours
Abstract
Cyclin A2 is an essential regulator of the cell division cycle through the activation of kinases that participate to the regulation of S phase as well as the mitotic entry. However, whereas its degradation by the proteasome in mid mitosis was thought to be essential for mitosis to proceed, recent observations show that a small fraction of cyclin A2 persists beyond metaphase and is degraded by autophagy. Its implication in the control of cytoskeletal dynamics and cell movement has unveiled its role in the modulation of RhoA activity. Since this GTPase is involved in both cell rounding early in mitosis and later, in the formation of the cleavage furrow, this suggests that cyclin A2 is a novel actor in cytokinesis. Taken together, these data point to this cyclin as a potential mediator of cell-niche interactions whose dysregulation could be taken as a hallmark of metastasis.
Core tip: Cyclin A2, as an essential regulator of the cell division cycle, is commonly associated to dividing cells and, like Ki67, is usually taken as a marker of cell proliferation. However, the level of this cyclin does not always correlate with the aggressiveness of the tumor, more particularly with respect to its invasiveness. Surprisingly, recent data suggest that it plays with RhoA also a role in the late phase of mitosis during which it is degraded by autophagy. Moreover, its dysregulation appears to be associated with the epithelial to mesenchymal transition.
