Cleavage of metastasis suppressor gene product KiSS-1 protein/metastin by matrix metalloproteinases

Takino, Takahisa; Koshikawa, Naohiko; Miyamori, Hisashi; Tanaka, Motohiro; Sasaki, Takuma; Okada, Yasunori; Seiki, Motoharu; Sato, Hiroshi

doi:10.1038/sj.onc.1206542

Cited by 138 publications

(125 citation statements)

References 31 publications

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“…27 KISS1 is able to diminish MMP9 expression by reducing nuclear factorkB binding to its promoter, 28 and it has been suggested that MMPs may serve as negative regulators of KISS1. 29 Our findings that demonstrate an inverse relationship between KISS1 expression and prognosis support the concept that KISS1 and MMP9 may somehow be related.…”

Section: Discussionsupporting

confidence: 81%

Expression of the metastasis suppressor gene KISS1 in uveal melanoma

Martins

Fernandes

Antecka

et al. 2008

Eye

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Purpose Uveal melanoma (UM) is the most common primary malignant intraocular tumour in adults. Forty-five percent of UM patients develop metastasis within 15 years of initial diagnosis. KISS1, a human metastasis suppressor gene, has been reported to play a role in various human malignancies. The purpose of this study was to investigate the expression of KISS1 in UM and its potential value as a prognostic marker. Methods Thirty-seven cases of paraffinembedded human UM specimens were immunostained with a KISS1 antibody. Clinical-pathological data were obtained. The relationship between the clinical-pathological data and the expression of KISS1 was evaluated. Moreover, the survival rates of the patients were also assessed. Five UM cell lines (92.1, OCM-1, MKTBR, UW1 and SP6.5) were assayed for KISS1 expression. In addition, real-time PCR was used to determine mRNA levels of KISS1 and its receptor GPR54 in these cell lines. Results The immunohistochemical results of KISS1 expression displayed cytoplasmic staining in 84% of UM specimens. Low KISS1 expression was associated with a higher risk of metastatic disease (Po0.05). Furthermore, we found that KISS1 was expressed in all five UM cells lines. Real-time PCR analysis confirmed the presence of both KISS1 and its receptor GPR54 in all five human UM cell lines. Conclusions To the best of our knowledge, this is the first time that KISS1 has been characterized in UM. The correlation between KISS1 expression and UM survival rate suggests an important role for KISS1 as a prognostic marker in this particular tumour.

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Section: Discussionsupporting

confidence: 81%

Expression of the metastasis suppressor gene KISS1 in uveal melanoma

Martins

Fernandes

Antecka

et al. 2008

Eye

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“…Interleukin receptor IL-2Rα no yes (Sheu et al, 2001) KiSS-1 protein/metastin yes yes (Takino et al, 2003) Kit-ligand yes (Heissig et al, 2002) Monocyte chemoattractant protein MCP-3 yes no (McQuibban et al, 2002) Monokine induced by interferon IFN-γ (MIG/CXCL -9) yes (Van den Myelin basic protein yes yes (Chandler et al, 1995) Myosin heavy chain yes yes (Rouet-Benzineb et al, 1999) Plasminogen yes yes (O'Reilly et al, 1999;Patterson and Sang, 1997) Platelet factor (PF)-4 yes…”

Section: (Van Den Steen Et Al 2003)mentioning

confidence: 99%

Gelatinase-mediated migration and invasion of cancer cells

Björklund

Koivunen

2005

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

465

609

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“…8 Cleavage of the KP 45−54 peptide between residues 51 and 52 by matrix metalloproteinases abolishes the activation of GPR-54 by the KP 45−54 peptide. 9 The KP 42−54 and KP 45−54 peptides also activate NPFF receptors, 10,11 and some of the actions of KP peptides could be mediated by NPFF receptor activation.There are profound changes in KP signaling at menopause 12 and notable sex differences in hypothalamic neurodegeneration in the elderly. 13 This correlates with a marked elevation of KP peptides in the hypothalamus of postmenopausal women that is not seen in males.…”

mentioning

confidence: 99%

“…9 The neuroprotective actions of the KP receptor antagonist P234 are additive to the protection observed with KP 42−54 and KP 45−50 and suggest that the neuroprotective mechanism is more complex. Since the P234 peptide is a derivative of KP 45−54 with modifications at residues 1, 5, and 8 and binds the KP receptor, it is possible that it has receptor activity as a partial agonist that is key to the neuroprotection observed but not to GnRH release.…”

mentioning

confidence: 99%

Kisspeptin Prevention of Amyloid-β Peptide Neurotoxicityin Vitro

Milton

Chilumuri

Rocha‐Ferreira

et al. 2012

ACS Chem. Neurosci.

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Alzheimer's disease (AD) onset is associated with changes in hypothalamic-pituitary−gonadal (HPG) function. The 54 amino acid kisspeptin (KP) peptide regulates the HPG axis and alters antioxidant enzyme expression. The Alzheimer's amyloid-β (Aβ) is neurotoxic, and this action can be prevented by the antioxidant enzyme catalase. Here, we examined the effects of KP peptides on the neurotoxicity of Aβ, prion protein (PrP), and amylin (IAPP) peptides. The Aβ, PrP, and IAPP peptides stimulated the release of KP and KP 45−54. The KP peptides inhibited the neurotoxicity of Aβ, PrP, and IAPP peptides, via an action that could not be blocked by kisspeptin-receptor (GPR-54) or neuropeptide FF (NPFF) receptor antagonists. Knockdown of KiSS-1 gene, which encodes the KP peptides, in human neuronal SH-SY5Y cells with siRNA enhanced the toxicity of amyloid peptides, while KiSS-1 overexpression was neuroprotective. A comparison of the catalase and KP sequences identified a similarity between KP residues 42−51 and the region of catalase that binds Aβ. The KP peptides containing residues 45−50 bound Aβ, PrP, and IAPP, inhibited Congo red binding, and were neuroprotective. These results suggest that KP peptides are neuroprotective against Aβ, IAPP, and PrP peptides via a receptor independent action involving direct binding to the amyloid peptides. KEYWORDS: KiSS-1, kisspeptin, amyloid-β, prion protein, amylin, neuroprotection N euroendocrine hormone changes are seen in aging, and there are disease specific changes associated with Alzheimer's disease (AD). 1,2 One of the neuroendocrine systems to show profound changes with aging is the hypothalamic−pituitary−gonadal (HPG) system, and the pathology of AD, Creutzfeldt−Jakob disease (CJD), and type 2 diabetes mellitus (T2DM) is also associated with changes in the hormones of this system. 3,4 A major regulator of the HPGaxis is the 54 amino acid kisspeptin (KP) peptide, which acts on gonadotrophin-releasing hormone (GnRH) neurons to activate GnRH release. 5 The KP peptide is produced in neurons by processing of the KiSS-1 preproprotein to yield the 54 amino acid KP peptide, which corresponds to residues 68−121 of KiSS-1. 6 Shorter derivatives of KP peptide comprising the C-terminal 14 (KP 41−54), 13 (KP 42−54), and 10 (KP 45−54) amino acids have also been found in tissues and corresponding to residues 108− 121, 109−121, and 112−121 of KiSS-1. 6,7 Biological activity of KP peptides requires the KP 45−54 sequence and is mediated via a specific KP receptor (GPR-54). 6,7 Lack of KP signaling via the GPR-54 receptor is associated with reproductive system failure. 8 Cleavage of the KP 45−54 peptide between residues 51 and 52 by matrix metalloproteinases abolishes the activation of GPR-54 by the KP 45−54 peptide. 9 The KP 42−54 and KP 45−54 peptides also activate NPFF receptors, 10,11 and some of the actions of KP peptides could be mediated by NPFF receptor activation.There are profound changes in KP signaling at menopause 12 and notable sex differences in hypothalamic neurodegenera...

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Cleavage of metastasis suppressor gene product KiSS-1 protein/metastin by matrix metalloproteinases

Cited by 138 publications

References 31 publications

Expression of the metastasis suppressor gene KISS1 in uveal melanoma

Expression of the metastasis suppressor gene KISS1 in uveal melanoma

Gelatinase-mediated migration and invasion of cancer cells

Kisspeptin Prevention of Amyloid-β Peptide Neurotoxicityin Vitro

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