Down-Regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Results in Mesenchymal-to-Epithelial Transition of Human Lung Fibrosarcoma Cells

Funasaka, Tatsuyoshi; Hu, Huankai; Yanagawa, Takashi; Hogan, Victor; Raz, Avraham

doi:10.1158/0008-5472.can-06-3935

Cited by 62 publications

(49 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…GPI expression is induced by hypoxia [52]. Its downregulation has been described to lead to mesenchymal to epithelial transition in lung cancer cells [53]. It is tempting to speculate that induction of GPI constitutes a link between aerobic glycolysis [54] and tumor cell motility.…”

Section: Introductionmentioning

confidence: 99%

Metastasis signatures: genes regulating tumor–microenvironment interactions predict metastatic behavior

Albini

Mirisola²,

Pfeffer³

2007

Cancer Metastasis Rev

View full text Add to dashboard Cite

The possibility of predicting clinical outcome of cancer patients through the analysis of gene expression profiles in the primary tumor is a kind of ideological revolution as the multistep carcinogenesis model postulates that the proportion of cells within the primary tumor that actually acquire metastasis driving mutation(s) is small; too small to leave its imprint on the gene expression profile. The data collected to date have brought a new paradigm to reality in the metastasis field: metastasis must at least in part rely on mutations and/or gene regulation events present in the majority of cells which constitute the primary tumor mass. By analyses of differential expression of primary tumors versus metastases or by functional analyses of putative metastasis genes in experimental metastasis, many metastasis-associated gene expression events have been identified that correlate with the development of metastases. Among genes "favoring" metastasis, we find many molecules that are expressed not by the tumor cell itself but by the cells of the microenvironment, as well as genes over-expressed in the primary tumor that have a principle role in mediating tumor-host interactions. Here we review these concepts and advance hypotheses on how gene expression of the primary tumor and the microenvironment can favor the spread of the metastasis seeds and how this knowledge can provide tools to secondary prevention.

show abstract

Section: Introductionmentioning

confidence: 99%

Metastasis signatures: genes regulating tumor–microenvironment interactions predict metastatic behavior

Albini

Mirisola²,

Pfeffer³

2007

Cancer Metastasis Rev

View full text Add to dashboard Cite

show abstract

“…rAMF Induces Cell Migration but Not Cell Proliferation in Two Melanoma Cell Lines (SBcl-2 and 1205Lu)-AMF is critical for the migration, invasion, metastasis, and anti-apoptotic effects of malignant tumor cells, and its multiple roles in tumor progression may be mediated by certain downstream pathways and effectors (2,5,6,8,(33)(34)(35). A previous study reported that melanoma cells secrete and respond to AMF in an autocrine manner with increased motility (2).…”

Section: Resultsmentioning

confidence: 99%

Phosphoglucose Isomerase/Autocrine Motility Factor Promotes Melanoma Cell Migration through ERK Activation Dependent on Autocrine Production of Interleukin-8

Araki

Shimura

Yajima

et al. 2009

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

It is well known that phosphoglucose isomerase/autocrine motility factor (AMF) promotes cell migration in an autocrine manner in various tumor cells. However, it remains unclear whether certain cytokines modulate the effects of AMF on tumor cell migration. Because interleukin (IL)-8, a proinflammatory cytokine, is produced by melanoma cells and has been correlated with melanoma migration, the migratory ability of melanoma cells induced by AMF may also involve induction of IL-8 expression. In the present study, we assessed whether AMF promotes melanoma cell migration through autocrine production of IL-8. We found that AMF stimulation increased IL-8 production through up-regulation of IL-8 mRNA transcription, especially in biologically early stage melanoma cells. AMF-induced migration of these cells was inhibited by a specific neutralizing antibody against IL-8. The IL-8 production induced by AMF was mediated by the ERK1/2 pathways. These findings suggest that melanoma migration induced by AMF is mediated by autocrine production of IL-8 as a novel downstream modulator of the AMF signaling pathway.

show abstract

“…Elevated serum AMF is found in patients with malignant tumors such as colorectal, lung, kidney, breast and gastrointestinal carcinomas and is well correlated with the development of metastasis (Iiizumi et al, 2008). Moreover, overexpression of AMF in normal fibroblasts lead to a gain of tumorigenicity (Funasaka et al, 2007). During tumor progression, an additional role of AMF is revealed, namely, it is demonstrated that AMF not only stimulates AMF-producing tumor cell motility in an autocrine manner by binding to its receptor, but also acts as a paracrine factor for vein endothelial cells; when functioning as a paracrine factor, AMF induces angiogenesis by stimulating cell motility and upregulating its VEGFR expression, and it may facilitate metastasis by becoming more active at the metastasis phase (Funasaka et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Aberrant Expression of the Autocrine Motility Factor Receptor Correlates with Poor Prognosis and Promotes Metastasis in Gastric Carcinoma

Huang

Zhang²,

Zha³

et al. 2014

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

AMFR, autocrine motility factor receptor, also called gp78, is a cell surface cytokine receptor which has a dual role as an E3 ubiquitin ligase in endoplasmic reticulum-associated degradation. AMFR expression is associated with tumor malignancy. We here investigated the clinical significance of AMFR and its role in metastasis and prognosis in gastric cancer. Expression of AMFR, E-cadherin and N-cadherin in cancer tissues and matched adjacent normal tissues from 122 gastric cancer (GC) patients undergoing surgical resection was assessed by immunohistochemistry. Levels of these molecules in 17 cases selected randomly were also analysed by Western blotting. AMFR expression was significantly increased in gastric cancer tissues, and associated with invasion depth and lymph node metastasis. Kaplan-Meier analysis showed AMFR expression correlated with poor overall survival and an increased risk of recurrence in the GC cases. Cox regression analysis suggested AMFR to be an independent predictor for overall and recurrence-free survival. E-cadherin expression was decreased in gastric cancer tissues; conversely, N-cadherin was increased. Expression of AMFR negatively correlated with E-cadherin expression, whereas N-cadherin expression showed a significant positive correlation with AMFR expression. AMFR might be involved in the regulation of epithelial-mesenchymal transition, with aberrant expression correlating with a poor prognosis and promoting invasion and metastasis in GCs.

show abstract

Down-Regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Results in Mesenchymal-to-Epithelial Transition of Human Lung Fibrosarcoma Cells

Cited by 62 publications

References 38 publications

Metastasis signatures: genes regulating tumor–microenvironment interactions predict metastatic behavior

Metastasis signatures: genes regulating tumor–microenvironment interactions predict metastatic behavior

Phosphoglucose Isomerase/Autocrine Motility Factor Promotes Melanoma Cell Migration through ERK Activation Dependent on Autocrine Production of Interleukin-8

Aberrant Expression of the Autocrine Motility Factor Receptor Correlates with Poor Prognosis and Promotes Metastasis in Gastric Carcinoma

Contact Info

Product

Resources

About