Selective migration of neuralized embryonic stem cells to stem cell factor and media conditioned by glioma cell lines

Serfózó, Péter; Schlarman, Maggie S; Pierret, Chris; Maria, Bernard L.; Kirk, Mark D.

doi:10.1186/1475-2867-6-1

Cited by 34 publications

(16 citation statements)

References 42 publications

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“…Likewise, c-kit has been identified as a marker of normal stem cells, such as hematopoietic and neural crest cells, as well as in several cancers, including glioma and neuroblastoma [33,34]. In neural crest stem cells, from which neuroblastomas arise, c-kit has been shown to support stem cell survival and has been suggested to play a role in the growth regulation of neuroblastoma [35].…”

Section: Discussionmentioning

confidence: 99%

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A distinct gene expression signature characterizes human neuroblastoma cancer stem cells

et al. 2015

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Section: Discussionmentioning

confidence: 99%

“…In neural crest stem cells, from which neuroblastomas arise, c-kit has been shown to support stem cell survival and has been suggested to play a role in the growth regulation of neuroblastoma [35]. Other studies have delineated a role for c-kit in glioma cell migration/metastasis and radioresistance [34,36]. …”

Section: Discussionmentioning

confidence: 99%

A distinct gene expression signature characterizes human neuroblastoma cancer stem cells

et al. 2015

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“…With regard to the risk of developing cancer, p27 exhibits a set of unique characteristics that are not seen in any other G1-to-S phase cell cycle regulatory proteins [14–16]. First, a relatively large number of nutritional and chemopreventive anti-cancer agents specifically increase the expression of p27 without directly affecting the expression of any other G1-to-S phase cell cycle regulatory proteins including INK4s, p57(Kip2), p21(Cip1Waf1), D-type cyclins, cyclin E, cyclin A, CDK2, CDK4 and CDK6 [14].…”

Section: Introductionmentioning

confidence: 99%

“…First, a relatively large number of nutritional and chemopreventive anti-cancer agents specifically increase the expression of p27 without directly affecting the expression of any other G1-to-S phase cell cycle regulatory proteins including INK4s, p57(Kip2), p21(Cip1Waf1), D-type cyclins, cyclin E, cyclin A, CDK2, CDK4 and CDK6 [14]. Second, the degree of increase in the expression of p27 in human breast adenocarcinoma cells in vitro is linearly and positively associated with the degree of inhibition of methylnitrosourea (MNU)-induced rat mammary adenocarcinoma in vivo [15].…”

Section: Introductionmentioning

confidence: 99%

“…This association, of course, does not exist for some anti-cancer agents that could not be converted to active anti-cancer metabolites in vitro . Lastly, unlike any other G1-to-S phase cell cycle regulatory proteins, expression of p27 is regulated primarily at the level of translation, not at the level of transcription [14–20]. For example, the level of expression of p27 “protein” oscillates significantly during the cell cycle, but the expression of p27 “mRNA” does not.…”

Section: Introductionmentioning

confidence: 99%

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Expression of p27Kip1, a cell cycle repressor protein, is inversely associated with potential carcinogenic risk in the genetic rodent models of obesity and long-lived Ames dwarf mice

Eto

2013

Metabolism

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Introduction The association of genetic rodent models of obesity and cancer still remains a controversial issue. Although this controversy has largely been resolved in recent years for homozygous leptin receptor-deficient obese Zucker rats and homozygous long-lived Ames dwarf mice, it is still unresolved for homozygous leptin-deficient obese ob/ob mice. Objective The objective of the present study described below was to investigate whether the expression of the cell cycle repressor protein p27(Kip1) is (a) down-regulated in the tumor-free homozygous leptin receptor-deficient obese Zucker rats as well as tumor-free homozygous leptin-deficient obese ob/ob mice and (b) up-regulated in the tumor-free homozygous long-lived Ames dwarf mice. Methods To achieve this objective, we first performed western immunoblot analysis of the hepatic expression of p27. We then performed western immunoblot analysis and proteomic analysis of the hepatic expression of the proteins involved in the upstream molecular signaling pathways for the expression of p27. Lastly, we analyzed the serum levels of glucose, insulin, and branched-chain amino acids, all of which have been shown to regulate, causally and inversely, the expression of p27. Results/Conclusions The results indicated that the hepatic expression of p27 was down-regulated in the homozygous leptin receptor-deficient obese Zucker rats and up-regulated in the homozygous long-lived Ames dwarf mice as expected. We also found that the hepatic expression of p27 was down-regulated in the homozygous leptin-deficient obese ob/ob mice. This last observation was not completely consistent with all of the results of the published studies where homozygous leptin-deficient obese ob/ob mice were used.

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Involvement of Cx43 phosphorylation in 5′‐N‐ethylcarboxamide‐induced migration and proliferation of mouse embryonic stem cells

Kim¹,

Lee²,

Han³

2010

Journal Cellular Physiology

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Despite a lot of gap junction research, the complex connection between gap junction and cell proliferation remains an exciting area of investigation. Thus, we examined the effect of connexin 43 (Cx43) on the migration and proliferation of embryonic stem (ES) cells and its related signaling pathways following stimulation with the adenosine analogue 5'-N-ethylcarboxamide (NECA). NECA increased phosphorylation of Cx43 which was blocked by caffeine, a non-selective adenosine receptor antagonist. In experiment to measure the gap junctional intercellular communication, NECA blocked transfer of Lucifer yellow to neighboring cells in a scrape loading/dye transfer (SL/DT) assay. In addition, NECA-induced phosphorylation of phosphoinositide 3-kinase (PI3K)/Akt, protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and nuclear factor-kappa B (NF-kappaB) signal pathways. Inhibition of these signaling pathways reduced NECA-induced phosphorylation of Cx43. Moreover, NECA-treated cells demonstrated phosphorylation of Src, which was blocked by caffeine. In this experiment, a disruption of Cx43 using Cx43-specific small interfering RNA (siRNA) also enhanced Src phosphorylation. In a further study, phosphorylations of integrin beta1, focal adhesion kinase (FAK), and paxillin by NECA were restrained by caffeine as well as the Src blocker, PP2. Finally, we identified that NECA-stimulated cell migration and expressions of cell-cycle regulatory proteins [cyclin D1, cyclin-dependent kinase (CDK) 4, cyclin E, and CDK2]; these increases were inhibited by caffeine, or PP2. We conclude that NECA-stimulated Cx43 phosphorylation mediated by PI3K/Akt, PKC, MAPKs, and NF-kappaB, which subsequently stimulated cell migration and proliferation through Src, integrin beta1, FAK, and paxillin signal pathways.

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Selective migration of neuralized embryonic stem cells to stem cell factor and media conditioned by glioma cell lines

Cited by 34 publications

References 42 publications

A distinct gene expression signature characterizes human neuroblastoma cancer stem cells

A distinct gene expression signature characterizes human neuroblastoma cancer stem cells

Expression of p27Kip1, a cell cycle repressor protein, is inversely associated with potential carcinogenic risk in the genetic rodent models of obesity and long-lived Ames dwarf mice

Involvement of Cx43 phosphorylation in 5′‐N‐ethylcarboxamide‐induced migration and proliferation of mouse embryonic stem cells

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