CD29 integrin‐ and LIMK1/cofilin‐mediated actin reorganization regulates the migration of haematopoietic progenitor cells underneath bone marrow stromal cells

Konakahara, Shu; Ohashi, Kazumasa; Mizuno, Kensaku; Itoh, Katsuhiko; Tsuji, Takashi

doi:10.1111/j.1356-9597.2004.00726.x

Cited by 25 publications

(19 citation statements)

References 62 publications

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“…For instance, the large magnupodium moving underneath MSCs might act as a searching-sensor process to guide HSPCs to an appropriate microenvironment ( fig. 1 e-h) [Konakahara et al, 2004;Wagner et al, 2005;Freund et al, 2006b]. The observation that similar plasma membrane protrusions (named proteopodia), which are themselves highly motile even when the cells are not in rapid motion, were induced by the chemotactic factor SDF-1 is in agreement with such a function [Frimberger et al, 2001].…”

Section: Cell Shape and Migrationsupporting

confidence: 67%

“…The concentration of prominin-1 in GM 1 -rich, but not GM 3 -rich membrane microdomains appears to be a general phenomenon, since a similar event occurs in polarized epithelial cells . Therefore, the polarization of migrating HSPCs might be driven not only by cytoskeleton remodeling directed, for instance, by small Rho GTPase [Giebel et al, 2004;Konakahara et al, 2004;Cancelas et al, 2006;Ghiaur et al, 2006;Yang et al, 2007], but also by a reorganization of their plasma membrane in terms of lipid microdomains. The latter might be required to concentrate and/or retain a particular set of membrane proteins in a given subdomain, such as uropod or leading edge.…”

Section: Cell Shape and Migrationmentioning

confidence: 99%

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New Insights into the Cell Biology of Hematopoietic Progenitors by Studying Prominin-1 (CD133)

Bauer

Fonseca²,

Florek³

et al. 2007

Cells Tissues Organs

124

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Prominin-1 (alias CD133) has received considerable interest because of its expression by several stem and progenitor cells originating from various sources, including the neural and hematopoietic systems. As a cell surface marker, prominin-1 is now used for somatic stem cell isolation. Its expression in cancer stem cells has broadened its clinical value, as it might be useful to outline new prospects for more effective cancer therapies by targeting tumor-initiating cells. Cell biological studies of this molecule have demonstrated that it is specifically concentrated in various membrane structures that protrude from the planar areas of the plasmalemma. Prominin-1 binds to the plasma membrane cholesterol and is associated with a particular membrane microdomain in a cholesterol-dependent manner. Although its physiological function is not yet determined, it is becoming clear that this cell surface protein, as a unique marker of both plasma membrane protrusions and membrane microdomains, might reveal new aspects of the cell biology of rare stem and cancer stem cells. The aim of this review is to outline the recent discoveries regarding the dynamic reorganization of the plasma membrane of rare CD133+ hematopoietic progenitor cells during cell migration and division.

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Section: Cell Shape and Migrationsupporting

confidence: 67%

Section: Cell Shape and Migrationmentioning

confidence: 99%

New Insights into the Cell Biology of Hematopoietic Progenitors by Studying Prominin-1 (CD133)

Bauer

Fonseca²,

Florek³

et al. 2007

Cells Tissues Organs

124

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“…Previous studies have indicated that profilin and cofilin have key roles in regulating the assembly of actin filaments beneath the plasma membrane, in order to promote cell motility and other actin-associated processes (45,46). Profilin-1 is an actin monomer-binding protein considered to be an essential factor in actin polymerization (47,48).…”

Section: Discussionmentioning

confidence: 99%

Regulation of cell migration via the EGFR signaling pathway in oral squamous cell carcinoma cells

et al. 2016

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Abstract. Cell migration potency is essential in cancer metastasis and is often regulated by extracellular stimuli. Oral squamous cell carcinoma cell lines include those that are sensitive, as well as resistant, to the effects of the epidermal growth factor receptor (EGFR) inhibitor cetuximab on cell migration. In the present study, the molecular differences in the EGFR response to cell migration between the SAS cetuximab-sensitive and HSC4 cetuximab-resistant cell lines was examined. Treatment with the EGFR inhibitors AG1478 and cetuximab reduced the migration potency of SAS cells, but not HSC4 cells. The migration of the two cell lines was inhibited under serum-free culture conditions, and the addition of EGF to the serum-free medium promoted the migration of SAS cells, but not HSC4 cells. In addition, SAS cell migration was reduced by the mitogen-activated protein kinase kinase and protein kinase B (Akt) inhibitors PD98059 and MK2206, whereas HSC4 cell migration was only inhibited by MK2206. EGF induced an increase in extracellular signal-regulated kinase phosphorylation levels in HSC4 cells, and stimulated Akt phosphorylation levels in SAS cells. Furthermore, the staining of actin filaments with phalloidin was significantly increased by the inhibition of EGFR in SAS cells, but was not observed as altered in HSC4 cells. Conversely, the addition of EGF to the culture medium decreased the accumulation of actin filaments in SAS cells. The results suggest that the EGF-EGFR signaling pathway has an important role in SAS cell migration via the modulation of actin dynamics, and that HSC4 cell migration is regulated by a serum component other than EGFR.

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“…It is not clear whether this additional effect of Ntn-1 in promoting cytoskeletal reorganization is a sequential result of the loss of cell cohesion or, alternatively, an independent process involving other cellular signaling events. However, it is clearly shown that Profilin-1 and Cofilin-1 play key roles in enhancing the actin assembly at the plasma membrane, thereby increasing F-actin expression that drives cell motility and other actin-linked processes [46,47]. Specifically, a-Actinins cross-links F-actin into bundles to form a cytoskeletal network [48].…”

Section: Effect Of Netrin-1 On Human Ucb-msc Motilitymentioning

confidence: 99%

Netrin-1 Induces MMP-12-Dependent E-Cadherin Degradation Via the Distinct Activation of PKCα and FAK/Fyn in Promoting Mesenchymal Stem Cell Motility

Lee

Jung

et al. 2014

Stem Cells and Development

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Netrin-1 (Ntn-1) is a potent inducer of neuronal cell migration; however, its molecular mechanism that guides the migratory behavior of stem cells has not been characterized. In this study, we investigate the role of Ntn-1 in promoting the motility of human umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs) and its related signaling pathways. Ntn-1 (50 ng/mL) significantly increased motility of UCB-MSCs, which was inhibited by blocking antibodies for deleted in colorectal cancer (DCC) and integrin (IN) a6b4. Ntn-1 in DCC stimulated protein kinase Ca (PKCa) activation, but not PKCe, PKCy, and PKCz, while Ntn-1 in INa6b4 induced the phosphorylation of focal adhesion kinase (FAK) and Fyn. Notably, Ntn-1 induced phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases ( JNK), and nuclear factor kappa-B (NF-kB), but they were concurrently downregulated by blocking the activities of PKCa, FAK, and Fyn. Ntn-1 uniquely increased the MMP-12 expression of all the matrix metalloproteinase (MMP) isoforms present in UCB-MSCs, though this was significantly blocked by an NF-kB inhibitor. Finally, Ntn-1 induced the MMP-12-dependent degradation of E-cadherin (E-cad), while Ntn-1 abrogated the interaction between E-cad and p120-catenin. In addition, Ntn-1 has the ability to stimulate cytoskeletal reorganization-related proteins, such as Cdc42, Rac1, Profilin-1, Cofilin-1, a-Actinin-4, and filamentous actin (F-actin) in UCB-MSCs. These results demonstrate that Ntn-1 induces MMP-12-dependent E-cad degradation via the distinct activation of PKCa and FAK/Fyn, which is necessary to govern the activation of ERK, JNK, and NF-kB in promoting motility of UCBMSCs.

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CD29 integrin‐ and LIMK1/cofilin‐mediated actin reorganization regulates the migration of haematopoietic progenitor cells underneath bone marrow stromal cells

Cited by 25 publications

References 62 publications

New Insights into the Cell Biology of Hematopoietic Progenitors by Studying Prominin-1 (CD133)

New Insights into the Cell Biology of Hematopoietic Progenitors by Studying Prominin-1 (CD133)

Regulation of cell migration via the EGFR signaling pathway in oral squamous cell carcinoma cells

Netrin-1 Induces MMP-12-Dependent E-Cadherin Degradation Via the Distinct Activation of PKCα and FAK/Fyn in Promoting Mesenchymal Stem Cell Motility

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