Hela l-CaD Is Implicated in the Migration of Endothelial Cells/Endothelial Progenitor Cells in Human Neoplasms

Zheng, Peng; Weiden, Marcel van der; Kros, Johan M.

doi:10.4161/cam.1.2.4332

Cited by 18 publications

(27 citation statements)

References 57 publications

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“…S2). Disassembly of vinculin-and talin-containing focal adhesions was observed in HeLa-l-CaD-positive endothelial cells (Zheng et al, 2007). Overexpression of l-CaD promotes cell movement, but inhibits cell contractility with a decrease in focal adhesions (Helfman et al, 1999).…”

Section: Discussionmentioning

confidence: 97%

“…Moreover, CaD expression induced by p53 suppresses Src-kinase-dependent podosome formation, which inhibits fibroblast and rat aortic SMC migration (Mukhopadhyay et al, 2009). By contrast, HeLa-l-CaD expression in endothelial cells and endothelial progenitor cells in the vasculature of various human tumors promotes cell migration for vasculogenesis and angiogenesis during tumor development (Zheng et al, 2004;Zheng et al, 2007). Of note, we observed that endogenous CaD in C2C12 myoblasts localized to the membrane ruffles, suggesting that CaD is involved in cell migration in C2C12 myoblasts.…”

Section: Discussionmentioning

confidence: 99%

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Sox4-mediated caldesmon expression facilitates skeletal myoblast differentiation

Jang

Kim

et al. 2013

Journal of Cell Science

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Summary Caldesmon (CaD), which was originally identified as an actin-regulatory protein, is involved in the regulation of diverse actin-related signaling processes, including cell migration and proliferation, in various cells. The cellular function of CaD has been studied primarily in the smooth muscle system; nothing is known about its function in skeletal muscle differentiation. In this study, we found that the expression of CaD gradually increased as differentiation of C2C12 myoblasts progressed. Silencing of CaD inhibited cell spreading and migration, resulting in a decrease in myoblast differentiation. Promoter analysis of the caldesmon gene (Cald1) and gel mobility shift assays identified Sox4 as a major trans-acting factor for the regulation of Cald1 expression during myoblast differentiation. Silencing of Sox4 decreased not only CaD protein synthesis but also myoblast fusion in C2C12 cells and myofibril formation in mouse embryonic muscle. Overexpression of CaD in Sox4-silenced C2C12 cells rescued the differentiation process. These results clearly demonstrate that CaD, regulated by Sox4 transcriptional activity, contributes to skeletal muscle differentiation.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Sox4-mediated caldesmon expression facilitates skeletal myoblast differentiation

Jang

Kim

et al. 2013

Journal of Cell Science

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“…CaD is an inhibitor of cell motility, and manipulation of CaD expression affects migration of several cell types (Mirzapoiazova et al, 2005;Yokouchi et al, 2006;Zheng et al, 2007). For example, increased CaD expression in human lung carcinoma A549 cells enhances stress fiber formation and reduces cell motility, whereas CaD depletion increases motility (Mayanagi et al, 2008).…”

Section: Phosphorylation Of Caldesmon By Pkgi Disrupts Its Interactiomentioning

confidence: 99%

cGMP-dependent Protein Kinase Iβ Regulates Breast Cancer Cell Migration and Invasion via a Novel Interaction with the Actin/Myosin-associated Protein Caldesmon

Schwappacher

Rangaswami

Su-Yuo

et al. 2013

Journal of Cell Science

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SummaryThe two isoforms of type I cGMP-dependent protein kinase (PKGIa and PKGIb) differ in their first ,100 amino acids, giving each isoform unique dimerization and autoinhibitory domains. The dimerization domains form coiled-coil structures and serve as platforms for isoform-specific protein-protein interactions. Using the PKGIb dimerization domain as an affinity probe in a proteomic screen, we identified the actin/myosin-associated protein caldesmon (CaD) as a PKGIb-specific binding protein. PKGIb phosphorylated human CaD on serine 12 in vitro and in intact cells. Phosphorylation on serine 12 or mutation of serine 12 to glutamic acid (S12E) reduced the interaction between CaD and myosin IIA. Because CaD inhibits myosin ATPase activity and regulates cell motility, we examined the effects of PKGIb and CaD on cell migration and invasion. Inhibition of the NO/cGMP/PKG pathway reduced migration and invasion of human breast cancer cells, whereas PKG activation enhanced their motility and invasion. siRNA-mediated knockdown of endogenous CaD had pro-migratory and pro-invasive effects in human breast cancer cells. Reconstituting cells with wild-type CaD slowed migration and invasion; however, CaD containing a phospho-mimetic S12E mutation failed to reverse the pro-migratory and pro-invasive activity of CaD depletion. Our data suggest that PKGIb enhances breast cancer cell motility and invasive capacity, at least in part, by phosphorylating CaD. These findings identify a pro-migratory and pro-invasive function for PKGIb in human breast cancer cells, suggesting that PKGIb is a potential target for breast cancer treatment.

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“…Immunolabeling of the EPCs was done by IF staining on the specimens from the glioma patients. The staining procedure was as before (Zheng et al, 2007a, b, c). Following IF staining FISH was performed on cells in interphase with the use of Dual color Vysis®LSI® DNA probes (Abbott Laboratories, Abbott Park, IL) for EGFR/CEP7 and PTEN (10q23)/CEP10.…”

Section: Methodsmentioning

confidence: 99%

Intratumoral, not circulating, endothelial progenitor cells share genetic aberrations with glial tumor cells

Zheng

Weiden

Spek

et al. 2013

Journal Cellular Physiology

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Literature data indicate that glioma stem cells may give rise to both tumor cells and endothelial progenitor cells (EPCs). Malignant glioma patients usually have increased levels of circulating (EPCs) and these cells are known to contribute to the glioma neovasculature. In this study we compared the intratumoral and circulating EPCs of glioma patients for a set of common glioma genotypical aberrations (amplification of EGFR; deletion of PTEN and aneusomy of chromosomes 7 and 10). We found that the EPCs present in the tumor tissues, not the circulating EPCs, share genetic aberrations with the tumor cells. EPCs with EGFR amplification were found in 46% and with PTEN deletion in 36% of the cases. EPCs with polysomy 7 and monosomy 10 were detected in 56% and 38% of the cases while centrosomal abnormalities in EPCs were found in 68% of the cases. The presence of genetic aberrations of glioma cells in intratumoral EPCs may point to transdifferentiation of glioma stem cells into EPCs. However, the tissue specific CD133 splice variant of blood EPCs was detected in the glioma tissues but not in control brains, suggestive of a blood origin of at least part of the intratumoral EPCs. The findings highlight the complexity of the cellular constituents of glioma neovascularization which should be taken into account when developing anti-angiogenic strategies for gliomas.

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Hela l-CaD Is Implicated in the Migration of Endothelial Cells/Endothelial Progenitor Cells in Human Neoplasms

Cited by 18 publications

References 57 publications

Sox4-mediated caldesmon expression facilitates skeletal myoblast differentiation

Sox4-mediated caldesmon expression facilitates skeletal myoblast differentiation

cGMP-dependent Protein Kinase Iβ Regulates Breast Cancer Cell Migration and Invasion via a Novel Interaction with the Actin/Myosin-associated Protein Caldesmon

Intratumoral, not circulating, endothelial progenitor cells share genetic aberrations with glial tumor cells

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