Tumour-cell migration, invasion, and metastasis: navigation by neurotransmitters

Entschladen, Frank; Drell, Theodore L.; Lang, Kerstin; Joseph, Jan; Zaenker, Kurt S.

doi:10.1016/s1470-2045(04)01431-7

Cited by 305 publications

(231 citation statements)

References 39 publications

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“…This secondary messenger, cAMP, regulates many cellular functions through its effectors, such as cAMP-dependent protein kinase (PKA) and EPAC (exchange proteins directly activated by cAMP) [69][70][71]. Preclinical studies have demonstrated that β-adrenergic signaling can regulate multiple fundamental biological processes underlying the progression and metastasis of tumors, including the promotion of inflammation [72][73][74], angiogenesis [75][76][77][78], migration [79], invasion [80,81] and resistance to programmed cell death [82][83][84][85]. Some evidence suggests that the stimulation of β-adrenergic signaling can also inhibit DNA damage repair and the cellular immune response [86,87] and promote surgery-induced metastasis [88,89].…”

Section: β-Adrenergic Signalingmentioning

confidence: 99%

Wnt3a Expression is Associated with MMP-9 Expression in Primary Tumor and Metastatic Site in Recurrent or Stage IV Colorectal Cancer

2014

Cancer Cell Signaling

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Infantile hemangioma (IH), which is the most common tumor in infants, is a benign vascular neoplasm resulting from the abnormal proliferation of endothelial cells and pericytes. For nearly a century, researchers have noted that IH exhibits diverse and often dramatic clinical behaviors. On the one hand, most lesions pose no threat or potential for complication and resolve spontaneously without concern in most children with IH. On the other hand, approximately 10% of IHs are destructive, disfiguring and even vision-or life-threatening. Recent studies have provided some insight into the pathogenesis of these vascular tumors, leading to a better understanding of the biological features of IH and, in particular, indicating that during hemangioma neovascularization, two main pathogenic mechanisms prevail, angiogenesis and vasculogenesis. Both mechanisms have been linked to alterations in several important cellular signaling pathways. These pathways are of interest from a therapeutic perspective because targeting them may help to reverse, delay or prevent hemangioma neovascularization. In this review, we explore some of the major pathways implicated in IH, including the VEGF/VEGFR, Notch, β-adrenergic, Tie2/angiopoietins, PI3K/AKT/mTOR, HIF-α-mediated and PDGF/PDGF-R-β pathways. We focus on the role of these pathways in the pathogenesis of IH, how they are altered and the consequences of these abnormalities. In addition, we review the latest preclinical and clinical data on the rationally designed targeted agents that are now being directed against some of these pathways.

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Section: β-Adrenergic Signalingmentioning

confidence: 99%

Wnt3a Expression is Associated with MMP-9 Expression in Primary Tumor and Metastatic Site in Recurrent or Stage IV Colorectal Cancer

2014

Cancer Cell Signaling

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“…Metastasis formation involves migration of malignant cells from the primary tumour via lymphatic or blood vessel routes with the process being tightly regulated by exogenous cell signalling molecules, including ligands to G protein-coupled receptors (GPCRs) such as neurotransmitters and chemokines [9,10]. In previous in vitro cell migration studies we have shown that the stress catecholamine hormone norepinephrine is a potent inducer of migratory activity in carcinoma cell lines of colon [11], prostate [12], ovarian cancer cells [13] and breast [14] tissue origin, and this finding has been confirmed in a mouse model [15].…”

Section: Introductionmentioning

confidence: 99%

Beta-Blocker Drug Therapy Reduces Secondary Cancer Formation in Breast Cancer and Improves Cancer Specific Survival

et al. 2010

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AbstrAct:Laboratory models show that the beta-blocker, propranolol, can inhibit norepinephrine-induced breast cancer cell migration. We hypothesised that breast cancer patients receiving beta-blockers for hypertension would show reduced metastasis and improved clinical outcome. Three patient subgroups were identified from the medical records of 466 consecutive female patients (median age 57, range 28-71) with operable breast cancer and follow-up (>10 years). Two subgroups comprised 43 and 49 hypertensive patients treated with beta-blockers or other antihypertensives respectively, prior to cancer diagnosis. 374 patients formed a nonhypertensive control group. Metastasis development, disease free interval, tumour recurrence and hazards risk were statistically compared between groups. KaplanMeier plots were used to model survival and DM. Beta-blocker treated patients showed a significant reduction in metastasis development (p=0.026), tumour recurrence (p=0.001), and longer disease free interval (p=0.01). In addition, there was a 57% reduced risk of metastasis (Hazards ratio=0.430; 95% CI=0.200-0.926, p=0.031), and a 71% reduction in breast cancer mortality after 10 years (Hazards ratio=0.291; 95% CI=0.119-0.715, p=0.007). This proof-of-principle study showed beta-blocker therapy significantly reduces distant metastases, cancer recurrence, and cancer-specific mortality in breast cancer patients suggesting a novel role for beta-blocker therapy. A larger epidemiological study leading to randomised clinical trials is needed for breast and other cancer types including colon, prostate and ovary.

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“…Cancer invasion and metastasis, both integral components of cancer progression, require an active motile cell phenotype. Cell motility and invasion are tightly regulated by the growth factors, cytokines, and extracellular matrix components in the tumor microenvironment (1,2). Hyaluronic acid (HA), 4 a component of the extracellular matrix, is abundantly secreted from the stromal fibroblast of cancerous tissues in response to humoral factors derived from tumor cells (3).…”

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confidence: 99%

Mechanism of MTA1 Protein Overexpression-linked Invasion

Sankaran

Pakala

Nair

et al. 2012

Journal of Biological Chemistry

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Background: Although MTA1 is overexpressed in advanced human cancer, its role in cancer invasion and migration needs to be elucidated. Results: MTA1 transcriptionally stimulates expression of the hyaluronan-mediated motility receptor (HMMR) and consequently regulates cancer invasion and migratory function. Conclusion: HMMR is a mediator of MTA1-mediated invasion and motility. Significance: This is the first report connecting MTA1 with HMMR expression and function.

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Tumour-cell migration, invasion, and metastasis: navigation by neurotransmitters

Cited by 305 publications

References 39 publications

Wnt3a Expression is Associated with MMP-9 Expression in Primary Tumor and Metastatic Site in Recurrent or Stage IV Colorectal Cancer

Wnt3a Expression is Associated with MMP-9 Expression in Primary Tumor and Metastatic Site in Recurrent or Stage IV Colorectal Cancer

Beta-Blocker Drug Therapy Reduces Secondary Cancer Formation in Breast Cancer and Improves Cancer Specific Survival

Mechanism of MTA1 Protein Overexpression-linked Invasion

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