Polarity Reversal by Centrosome Repositioning Primes Cell Scattering during Epithelial-to-Mesenchymal Transition

Burute, Mithila; Prioux, Magali; Blin, Guillaume; Truchet, Sandrine; Letort, Gaëlle; Tseng, Qingzong; Bessy, Thomas; Lowell, Sally; Young, Joanne; Filhol, Odile; Théry, Manuel

doi:10.1016/j.devcel.2016.12.004

Cited by 93 publications

(108 citation statements)

References 85 publications

(116 reference statements)

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“…Because claudins play a role in cell-to-cell adhesion, Snail down-regulation of claudins induces EMT, in which the epithelial cells lose their polarity and their characteristic adhesion. 3,20,21,51 …”

Section: Indirect Regulation Of Emt By Yy1 Through the Nf-κb/snamentioning

confidence: 99%

“…1,2 EMT is the process through which epithelial cells lose their cell polarity and cell–cell adhesion to become migratory mesenchymal stem cells (MSCs). 3,4 EMT is a process that is crucial for cell differentiation during distinct stages of embryogenesis such as gastrulation, 4 but when dysregulated, can lead to negative outcomes in cancer due to the MSCs’ enhanced migratory capacity, invasiveness, and higher resistance to apoptosis compared with normal cells. 5 …”

Section: Introductionmentioning

confidence: 99%

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Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Cho

Bonavida

2017

Crit Rev Oncog

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There have been recent developments in the treatment of various cancers, in particular non-metastatic cancers. However, many of the responding patients often relapse initially through the development of spread micro-and macro-metastases. Unfortunately, there are very few therapeutic modalities for the treatment of metastatic cancers. The development of cancer metastasis has been proposed to involve the epithelial–mesenchymal transition (EMT), in which the tumor cells with the EMT phenotype exhibit various phenotypic markers and molecular modifications that are manifested to resist most conventional therapies. YY1 is a target of the hyperactivated nuclear factor-kappa beta pathway in cancer and it was reported that YY1 also regulates cell survival and cell proliferation in addition to its role in EMT and resistance. The overexpression of YY1 in the majority of cancers has been correlated with poor prognosis. It is hypothesized that targeting YY1 may result in several anti-tumor activities, including inhibition of cell survival and cell proliferation, inhibition of EMT, and reversal of resistance. This review discusses the potential therapeutic targeting of an overexpressed transcription factor, Yin Yang 1 (YY1), which has been implicated in the development of EMT and drug resistance. Several examples targeting YY1 in experimental models are presented.

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Section: Indirect Regulation Of Emt By Yy1 Through the Nf-κb/snamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Cho

Bonavida

2017

Crit Rev Oncog

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“…We developed quantitative imaging tools for measuring the emergence of epithelial organisation based on segmenting individual nuclei and centrosomes and measuring nucleus centrosome vectors relative to the cavity of the embryo ( Fig 1A) (Burute et al, 2017) https://pickcellslab.frama.io/docs/use/features/segmentation/nc_assignments/. We used this approach to assess the extent to which pluripotent cells are organised into an epithelium before and after implantation of the embryo.…”

Section: Pluripotent Cells Co-align Into An Epithelium As They Becomementioning

confidence: 99%

Competence to epithelialise coincides with competence to differentiate in pluripotent cells

Lin

Tatar

Blin

et al. 2019

Preprint

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Pluripotent cells reorganise themselves into an epithelium before they initiate differentiation, but it is not clear how these two events are mechanistically linked. Here we use quantitative imaging approaches to measure cellular rearrangements that accompany exit from naive pluripotency. We show that competence to epithelialise, like competence to differentiate, is a regulated process. The pro-differentiation transcription factor Tcf15 prospectively identifies cells that are competent to epithelialise. We identify early upregulation of the laminin receptor integrin alpha3 prior to differentiation and show that Tcf15 helps to regulate this change. Finally, we show that Tcf15 identifies and is required for efficient differentiation of a primed subpopulation of pluripotent cells.We conclude that competence to epithelialise is actively regulated and linked to differentiationcompetence through the transcription factor Tcf15.

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“…Microtubule stabilization has been shown to be essential for axon specification (Witte et al, 2008), though the mechanisms underlying its local control remain largely unknown (Kapitein and Hoogenraad, 2015). Because centrosome repositioning is also driven by microtubule stabilization (Burute et al, 2017;Pitaval et al, 2017), this suggests that such centrosome-associated microtubule stabilizers might function as key effectors linking centrosome position and axon outgrowth. In the BTNs, initial axon outgrowth is concurrent with migration: the leading edge of the BTNs extends and becomes the proximal (anterior) process of the axon.…”

Section: Saxo: Stabilizer Of Axonemal Microtubulesmentioning

confidence: 99%

Neurogenin regulates effectors of migratory neuron cell behaviors in Ciona

Gibboney

Kim

Razy-Krajka

et al. 2019

Preprint

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The bipolar tail neurons (BTNs) of Ciona develop according to a highly dynamic, yet highly stereotyped developmental program and thus could serve as an accessible model system for neuronal delamination, migration, and polarized axon outgrowth. Here we used FACS/RNAseq to profile the transcriptional output of Neurogenin in the BTNs, searching for candidate effectors of BTN cell behaviors. We identified several candidate genes that might play conserved roles in similar cell behaviors in other animals, including mammals. Among the more interesting candidates were several microtubule-binding proteins and TGFβ pathway antagonists. A small Gαi subunit was also found to be upregulated in migrating BTNs, and interfering with its function through expression of a dominant negative inhibited delamination and a complete epithelial-to-mesenchymal transition. We propose models for the regulation of BTN behaviors by the identified candidate effectors, establishing a foundation for testing effector gene functions that might be conserved in chordate neurodevelopment.

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Polarity Reversal by Centrosome Repositioning Primes Cell Scattering during Epithelial-to-Mesenchymal Transition

Cited by 93 publications

References 85 publications

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Competence to epithelialise coincides with competence to differentiate in pluripotent cells

Neurogenin regulates effectors of migratory neuron cell behaviors in Ciona

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