The CDC42-Interacting Protein 4 Controls Epithelial Cell Cohesion and Tumor Dissemination

Rolland, Yannève; Marighetti, Paola; Malinverno, Chiara; Confalonieri, Stefano; Luise, Chiara; Ducano, Nadia; Palamidessi, Andrea; Bisi, Sara; Kajiho, Hiroaki; Troglio, Flavia; Shcherbakova, Olga G.; Dunn, Alexander R.; Oldani, Amanda; Lanzetti, Letizia; Fiore, Pier Paolo Di; Disanza, Andrea; Scita, Giorgio

doi:10.1016/j.devcel.2014.08.006

Cited by 41 publications

(52 citation statements)

References 50 publications

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“…In fact, CIP4 promotes lamellipodia formation in cortical neurons (Saengsawang et al, 2012) and localizes at the leading edge in tumor cells (Pichot et al, 2010;Truesdell et al, 2014). A recent study has shown that CIP4 regulates cell cohesion by modulating E-cadherin endocytosis and the actomyosin contraction required to break cell-cell junctions, thus facilitating cell migration (Rolland et al, 2014). Therefore, previous studies support the hypothesis that CIP4 participates in cell migration through its canonical role in integrating membrane deformation and actin dynamics.…”

Section: Discussionsupporting

confidence: 69%

“…6C). Considering that CIP4 is involved in several processes related to cell migration, including the disassembly of the adherens junctions (Rolland et al, 2014), the mechanism involved in centrosome and Golgi polarization could be independent of the interaction of CIP4 with AKAP350. Therefore, we evaluated whether this interaction was relevant for centrosomal and Golgi polarization.…”

Section: Akap350 Recruits Cip4 To the Centrosome In Migrating Cellsmentioning

confidence: 99%

“…Therefore, CIP4 acts downstream of cdc42 activation to promote membrane deformation, vesicle scission and actin polymerization (Fricke et al, 2009), thus participating in endocytosis (Leibfried et al, 2008;Hartig et al, 2009;Feng et al, 2010), and in the formation of lamellapodial protrusions (Saengsawang et al, 2012) and pro-invasive invadopodia structures (Pichot et al, 2010;Hu et al, 2011). Regarding cell migration, CIP4 is upregulated during epithelial-mesenchymal transition (Zhang et al, 2013) and has been reported to be essential for the development of metastatic properties in different types of cancer cells (Pichot et al, 2010;Truesdell et al, 2014;Rolland et al, 2014;Koshkina et al, 2013). Although most studies point to its involvement in the formation of membrane structures that are necessary for cell migration, the actual mechanism by which CIP4 plays a central role in the acquisition of migratory properties has not been clarified yet.…”

Section: Introductionmentioning

confidence: 99%

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Centrosomal AKAP350 and CIP4 act in concert to define centrosome/Golgi polarity in migratory cells

Tonucci

Hidalgo

Ferretti

et al. 2015

Journal of Cell Science

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The acquisition of a migratory phenotype is central in processes as diverse as embryo differentiation and tumor metastasis. An early event in this phenomenon is the generation of a nucleuscentrosome-Golgi back-to-front axis. AKAP350 (also known as AKAP9) is a Golgi and centrosome scaffold protein that is involved in microtubule nucleation. AKAP350 interacts with CIP4 (also known as TRIP10), a cdc42 effector that regulates actin dynamics. The present study aimed to characterize the participation of centrosomal AKAP350 in the acquisition of migratory polarity, and the involvement of CIP4 in the pathway. The decrease in total or in centrosomal AKAP350 led to decreased formation of the nucleus-centrosomeGolgi axis and defective cell migration. CIP4 localized at the centrosome, which was enhanced in migratory cells, but inhibited in cells with decreased centrosomal AKAP350. A decrease in the CIP4 expression or inhibition of the CIP4-AKAP350 interaction also led to defective cell polarization. Centrosome positioning, but not nuclear movement, was affected by loss of CIP4 or AKAP350 function. Our results support a model in which AKAP350 recruits CIP4 to the centrosome, providing a centrosomal scaffold to integrate microtubule and actin dynamics, thus enabling centrosome polarization and ensuring cell migration directionality.

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Section: Discussionsupporting

confidence: 69%

Section: Akap350 Recruits Cip4 To the Centrosome In Migrating Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Centrosomal AKAP350 and CIP4 act in concert to define centrosome/Golgi polarity in migratory cells

Tonucci

Hidalgo

Ferretti

et al. 2015

Journal of Cell Science

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“…CIP4 is an effector of Cdc42, another Rho-like GTPase critical to actin dynamics, migration, and endocytosis that is also frequently altered in cancer. CIP4 overexpression in breast cancer represents an independent predictor of disease outcome, being associated with poorer prognosis and metastasis (15,16). Mechanistically, this is due to increased E-cadherin internalization leading to cell scattering and improved actomyosin contractility (16).…”

Section: Introductionmentioning

confidence: 99%

Behind the Scenes: Endo/Exocytosis in the Acquisition of Metastatic Traits

Lanzetti

Fiore

2017

Cancer Research

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Alterations of endo/exocytic proteins have long been associated with malignant transformation, and genes encoding membrane trafficking proteins have been identified as bona fide drivers of tumorigenesis. Focusing on the mechanisms underlying the impact of endo/exocytic proteins in cancer, a scenario emerges in which altered trafficking routes/networks appear to be preferentially involved in the acquisition of prometastatic traits. This involvement in metastasis frequently occurs through the integration of programs leading to migratory/invasive phenotypes, survival and resistance to environmental stresses, epithelial-to-mesenchymal transition, and the emergence of cancer stem cells. These findings might have important implications in the clinical setting for the development of metastasis-specific drugs and for patient stratification to optimize the use of available therapies.

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“…In contrast, HEK cells grown on elastic substrates into embryonic bodies exhibited higher actin tension than on glass, so did TGFb1-treated, hRas-transformed MDCK cells [27]. In mammary epithelial cells, epithelial growth factor (EGF) increased E-cadherin tension, presumably through a CIP4-dependent control of actomyosin contraction [47].…”

Section: Sensitivity To Extracellular Cuesmentioning

confidence: 96%

FRET-based Molecular Tension Microscopy

Gayrard

Borghi

2016

Methods

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Cells generate and experience mechanical forces that may shape tissues and regulate signaling pathways in a variety of physiological or pathological situations. How forces propagate and transduce signals at the molecular level is poorly understood. The advent of FRET-based Molecular Tension Microscopy now allows to achieve mechanical force measurements at a molecular scale with molecular specificity in situ, and thereby better understand the mechanical architecture of cells and tissues, and mechanotransduction pathways. In this review, we will first expose the basic principles of FRET-based MTM and its various incarnations. We will describe different ways of measuring FRET, their advantages and drawbacks. Then, throughout the range of proteins of interest, cells and organisms to which it has been applied, we will review the tests developed to validate the approach, how molecular tension was related to cell functions, and conclude with possible developments and offshoots.

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The CDC42-Interacting Protein 4 Controls Epithelial Cell Cohesion and Tumor Dissemination

Cited by 41 publications

References 50 publications

Centrosomal AKAP350 and CIP4 act in concert to define centrosome/Golgi polarity in migratory cells

Centrosomal AKAP350 and CIP4 act in concert to define centrosome/Golgi polarity in migratory cells

Behind the Scenes: Endo/Exocytosis in the Acquisition of Metastatic Traits

FRET-based Molecular Tension Microscopy

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