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Article ; Online: MET-Activating Ubiquitin Multimers.

Kawakami, Naoya / Sato, Hiroki / Terasaka, Naohiro / Matsumoto, Kunio / Suga, Hiroaki

Angewandte Chemie (International ed. in English)

2023 Volume 62, Issue 36, Page(s) e202307157

Abstract: Receptor tyrosine kinases (RTKs) are generally activated through their dimerization and/or oligomerization induced by their cognate ligands, and one such RTK hepatocyte growth factor (HGF) receptor, known as MET, plays an important role in tissue ... ...

Abstract	Receptor tyrosine kinases (RTKs) are generally activated through their dimerization and/or oligomerization induced by their cognate ligands, and one such RTK hepatocyte growth factor (HGF) receptor, known as MET, plays an important role in tissue regeneration. Here we show the development of ubiquitin (Ub)-based protein ligand multimers, referred to as U-bodies, which act as surrogate agonists for MET and are derived from MET-binding macrocyclic peptides. Monomeric Ub constructs (U-body) were first generated by genetic implantation of a macrocyclic peptide pharmacophore into a structural loop of Ub (lasso-grafting) and subsequent optimization of its flanking spacer sequences via mRNA display. Such U-body constructs exhibit potent binding affinity to MET, thermal stability, and proteolytic stability. The U-body constructs also partially/fully inhibited or enhanced HGF-induced MET-phosphorylation. Their multimerization to dimeric, tetrameric, and octameric U-bodies linked by an appropriate peptide linker yielded potent MET activation activity and downstream cell proliferation-promoting activity. This work suggests that lasso-grafting of macrocycles to Ub is an effective approach to devising protein-based artificial RTK agonists and it can be useful in the development of a new class of biologics for various therapeutic applications.
MeSH term(s)	Hepatocyte Growth Factor/metabolism ; Ubiquitin/metabolism ; Protein Binding ; Proto-Oncogene Proteins c-met/metabolism ; Phosphorylation ; Peptides/pharmacology ; Peptides/metabolism
Chemical Substances	Hepatocyte Growth Factor (67256-21-7) ; Ubiquitin ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Peptides
Language	English
Publishing date	2023-07-31
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2011836-3
ISSN	1521-3773 ; 1433-7851
ISSN (online)	1521-3773
ISSN	1433-7851
DOI	10.1002/anie.202307157
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Article ; Online: Dimer Interface in Natural Variant NK1 Is Dispensable for HGF-Dependent Met Receptor Activation.

Tahira, Yumiko / Sakai, Katsuya / Sato, Hiroki / Imamura, Ryu / Matsumoto, Kunio

International journal of molecular sciences

2021 Volume 22, Issue 17

Abstract: NK1, a splicing variant of hepatocyte growth factor (HGF), binds to and activates Met receptor by forming an NK1 dimer and 2:2 complex with Met. Although the structural mechanism underlying Met activation by HGF remains incompletely resolved, it has been ...

Abstract	NK1, a splicing variant of hepatocyte growth factor (HGF), binds to and activates Met receptor by forming an NK1 dimer and 2:2 complex with Met. Although the structural mechanism underlying Met activation by HGF remains incompletely resolved, it has been proposed that the NK1 dimer structure participates in this activation. We investigated the NK1 dimer interface's role in Met activation by HGF. Because N127, V140, and K144 are closely involved in the head-to-tail NK1 dimer formation, mutant NK1 proteins with replacement of these residues by alanine were prepared. In Met tyrosine phosphorylation assays, N127-NK1, V140-NK1, and K144-NK1 showed 8.3%, 23.8%, and 52.2% activity, respectively, compared with wild-type NK1. Although wild-type NK1 promoted cell migration and scattering, N127-NK1, V140-NK1, and K144-NK1 hardly or marginally promoted them, indicating loss of activity of these mutant NK1 proteins to activate Met. In contrast, mutant HGFs (N127-HGF, V140-HGF, and K144-HGF) with the same amino acid replacements as in NK1 induced Met tyrosine phosphorylation and biological responses at levels comparable to those of wild-type HGF. These results indicate that the structural basis responsible for NK1-dependent Met dimer formation and activation differs from, or is at least distinguishable from, the structural basis responsible for HGF-dependent Met activation.
MeSH term(s)	Animals ; Binding Sites ; Cell Line, Tumor ; Dogs ; HEK293 Cells ; Hepatocyte Growth Factor/chemistry ; Hepatocyte Growth Factor/genetics ; Hepatocyte Growth Factor/metabolism ; Humans ; Madin Darby Canine Kidney Cells ; Mutation ; Protein Binding ; Protein Multimerization ; Proto-Oncogene Proteins c-met/chemistry ; Proto-Oncogene Proteins c-met/metabolism ; Signal Transduction
Chemical Substances	Hepatocyte Growth Factor (67256-21-7) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2021-08-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22179240
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Article ; Online: Met receptor is essential for MAVS-mediated antiviral innate immunity in epithelial cells independent of its kinase activity.

Imamura, Ryu / Sato, Hiroki / Chih-Cheng Voon, Dominic / Shirasaki, Takayoshi / Honda, Masao / Kurachi, Makoto / Sakai, Katsuya / Matsumoto, Kunio

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 40, Page(s) e2307318120

Abstract: Epithelial tissue is at the forefront of innate immunity, playing a crucial role in the recognition and elimination of pathogens. Met is a receptor tyrosine kinase that is necessary for epithelial cell survival, proliferation, and regeneration. Here, we ... ...

Abstract	Epithelial tissue is at the forefront of innate immunity, playing a crucial role in the recognition and elimination of pathogens. Met is a receptor tyrosine kinase that is necessary for epithelial cell survival, proliferation, and regeneration. Here, we showed that Met is essential for the induction of cytokine production by cytosolic nonself double-stranded RNA through retinoic acid-inducible gene-I-like receptors (RLRs) in epithelial cells. Surprisingly, the tyrosine kinase activity of Met was dispensable for promoting cytokine production. Rather, the intracellular carboxy terminus of Met interacted with mitochondrial antiviral-signaling protein (MAVS) in RLR-mediated signaling to directly promote MAVS signalosome formation. These studies revealed a kinase activity-independent function of Met in the promotion of antiviral innate immune responses, defining dual roles of Met in both regeneration and immune responses in the epithelium.
MeSH term(s)	Epithelial Cells ; Receptor Protein-Tyrosine Kinases ; Immunity, Innate ; Antiviral Agents ; Cytokines
Chemical Substances	Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Antiviral Agents ; Cytokines
Language	English
Publishing date	2023-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2307318120
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Article ; Online: Rho family small GTPase Rif regulates Wnt5a-Ror1-Dvl2 signaling and promotes lung adenocarcinoma progression.

Nishita, Michiru / Kamizaki, Koki / Hoshi, Kyoka / Aruga, Kana / Nishikaku, Ikumi / Shibuya, Hiroshi / Matsumoto, Kunio / Minami, Yasuhiro

The Journal of biological chemistry

2023 Volume 299, Issue 10, Page(s) 105248

Abstract: Rho in filopodia (Rif), a member of the Rho family of small GTPases, induces filopodia formation primarily on the dorsal surface of cells; however, its function remains largely unclear. Here, we show that Rif interacts with Ror1, a receptor for Wnt5a ... ...

Abstract	Rho in filopodia (Rif), a member of the Rho family of small GTPases, induces filopodia formation primarily on the dorsal surface of cells; however, its function remains largely unclear. Here, we show that Rif interacts with Ror1, a receptor for Wnt5a that can also induce dorsal filopodia. Our immunohistochemical analysis revealed a high frequency of coexpression of Ror1 and Rif in lung adenocarcinoma. Lung adenocarcinoma cells cultured on Matrigel established front-rear polarity with massive filopodia on their front surfaces, where Ror1 and Rif were accumulated. Suppression of Ror1 or Rif expression inhibited cell proliferation, survival, and invasion, accompanied by the loss of filopodia and cell polarity in vitro, and prevented tumor growth in vivo. Furthermore, we found that Rif was required to activate Wnt5a-Ror1 signaling at the cell surface leading to phosphorylation of the Wnt signaling pathway hub protein Dvl2, which was further promoted by culturing the cells on Matrigel. Our findings reveal a novel function of Rif in mediating Wnt5a-Ror1-Dvl2 signaling, which is associated with the formation of polarized filopodia on 3D matrices in lung adenocarcinoma cells.
Language	English
Publishing date	2023-09-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2023.105248
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Article ; Online: Two-Chain Mature Hepatocyte Growth Factor-Specific Positron Emission Tomography Imaging in Tumors Using

Warashina, Shota / Sato, Hiroki / Zouda, Maki / Takahashi, Maiko / Wada, Yasuhiro / Passioura, Toby / Suga, Hiroaki / Watanabe, Yasuyoshi / Matsumoto, Kunio / Mukai, Hidefumi

Molecular pharmaceutics

2023 Volume 20, Issue 4, Page(s) 2029–2038

Abstract: Two-chain hepatocyte growth factor (tcHGF), the mature form of HGF, is associated with malignancy and anticancer drug resistance; therefore, its quantification is an important indicator for cancer diagnosis. In tumors, activated tcHGF hardly discharges ... ...

Abstract	Two-chain hepatocyte growth factor (tcHGF), the mature form of HGF, is associated with malignancy and anticancer drug resistance; therefore, its quantification is an important indicator for cancer diagnosis. In tumors, activated tcHGF hardly discharges into the systemic circulation, indicating that tcHGF is an excellent target for molecular imaging using positron emission tomography (PET). We recently discovered HGF-inhibitory peptide-8 (HiP-8) that binds specifically to human tcHGF with nanomolar affinity. The purpose of this study was to investigate the usefulness of HiP-8-based PET probes in human
MeSH term(s)	Mice ; Humans ; Animals ; Hepatocyte Growth Factor/metabolism ; Peptides/chemistry ; Neoplasms/diagnostic imaging ; Positron-Emission Tomography/methods ; Chelating Agents/chemistry ; Copper Radioisotopes/chemistry ; Cell Line, Tumor
Chemical Substances	Hepatocyte Growth Factor (67256-21-7) ; Peptides ; Chelating Agents ; Copper Radioisotopes
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2138405-8
ISSN	1543-8392 ; 1543-8384
ISSN (online)	1543-8392
ISSN	1543-8384
DOI	10.1021/acs.molpharmaceut.2c01020
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Article ; Online: Hepatocyte growth factor in physiology and infectious diseases.

Imamura, Ryu / Matsumoto, Kunio

Cytokine

2017 Volume 98, Page(s) 97–106

Abstract: Hepatocyte growth factor (HGF) is a pleiotropic cytokine composed of an α-chain and a β-chain, and these chains contain four kringle domains and a serine protease-like structure, respectively. The receptor for HGF was identified as the c-met proto- ... ...

Abstract	Hepatocyte growth factor (HGF) is a pleiotropic cytokine composed of an α-chain and a β-chain, and these chains contain four kringle domains and a serine protease-like structure, respectively. The receptor for HGF was identified as the c-met proto-oncogene product of transmembrane receptor tyrosine kinase. HGF-induced signaling through the receptor Met provokes dynamic biological responses that support morphogenesis, regeneration, and the survival of various cells and tissues, which includes hepatocytes, renal tubular cells, and neurons. Characterization of tissue-specific Met knockout mice has further indicated that the HGF-Met system modulates immune cell functions and also plays an inhibitory role in the progression of chronic inflammation and fibrosis. However, the biological actions that are driven by the HGF-Met pathway all play a role in the acquisition of the malignant characteristics in tumor cells, such as invasion, metastasis, and drug resistance in the tumor microenvironment. Even though oncogenic Met signaling remains the major research focus, the HGF-Met axis has also been implicated in infectious diseases. Many pathogens try to utilize host HGF-Met system to establish comfortable environment for infection. Their strategies are not only simply change the expression level of HGF or Met, but also actively hijack HGF-Met system and deregulating Met signaling using their pathogenic factors. Consequently, the monitoring of HGF and Met expression, along with real-time detection of Met activation, can be a beneficial biomarker of these infectious diseases. Preclinical studies designed to address the therapeutic significance of HGF have been performed on injury/disease models, including acute tissue injury, chronic fibrosis, and cardiovascular and neurodegenerative diseases. Likewise, manipulating the HGF-Met system with complete control will lead to a tailor made treatment for those infectious diseases.
Language	English
Publishing date	2017-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2016.12.025
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Article: Dual blockade of MET and VEGFR2 signaling pathways as a potential therapeutic maneuver for peritoneal carcinomatosis in scirrhous gastric cancer

Kasai, Suguru / Kuwayama, Naomi / Motoo, Yoshiharu / Kawashima, Atsuhiro / Matsumoto, Kunio / Yano, Seiji / Matsushima, Kouji / Yasumoto, Kazuo

Biochemical and biophysical research communications. 2022 Apr. 16, v. 600

2022

Abstract: Scirrhous gastric cancer frequently develops into peritoneal carcinomatosis with malignant ascites, leading to an extremely poor prognosis. We had demonstrated that paracrine hepatocyte growth factor (HGF)-induced MET activation promotes peritoneal ... ...

Abstract	Scirrhous gastric cancer frequently develops into peritoneal carcinomatosis with malignant ascites, leading to an extremely poor prognosis. We had demonstrated that paracrine hepatocyte growth factor (HGF)-induced MET activation promotes peritoneal carcinomatosis with ascites formation. The vascular endothelial growth factor (VEGF) receptor (VEGFR)/VEGF axis facilitates tumor progression and formation of malignant ascites. This study investigated the role of MET and VEGFR2 in the development of peritoneal carcinomatosis with malignant ascites. Cabozantinib is a dual inhibitor of MET and VEGFR2. We examined the effects of cabozantinib on MET- and VEGFR2-mediated progression of peritoneal carcinomatosis in human scirrhous gastric cancer in vitro and in vivo. Cabozantinib inhibited HGF-stimulated proliferation of scirrhous cancer cell lines NUGC4 and GCIY, with a high potential to generate peritoneal carcinomatosis with ascites fluid, as well as the constitutive proliferation of MKN45 cells with MET amplification. Cabozantinib also inhibited the phosphorylation of both MET and VEGFR2 in scirrhous cancer cells and HGF- or VEGF-stimulated HUVECs. It effectively reduced ascitic fluid and prolonged the survival of NUGC4-inoculated nude mice. In clinical specimens, malignant ascites fluid from patients with peritoneal carcinomatosis contained high levels of HGF and VEGF. Our results strongly suggest that MET- and VEGFR2-mediated signaling pathways play pivotal roles in the pathogenesis of peritoneal carcinomatosis in scirrhous gastric cancer. Thus, the dual blockade of MET and VEGFR2 signaling may be a potential therapeutic maneuver for peritoneal carcinomatosis in scirrhous gastric cancer.
Keywords	ascites ; hepatocyte growth factor ; humans ; neoplasm cells ; neoplasm progression ; phosphorylation ; prognosis ; research ; stomach neoplasms ; therapeutics ; vascular endothelial growth factor receptor-2 ; vascular endothelial growth factors
Language	English
Dates of publication	2022-0416
Size	p. 80-86.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.02.045
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cyclic Peptide-Based Biologics Regulating HGF-MET.

Sato, Hiroki / Imamura, Ryu / Suga, Hiroaki / Matsumoto, Kunio / Sakai, Katsuya

International journal of molecular sciences

2020 Volume 21, Issue 21

Abstract: Using a random non-standard peptide integrated discovery system, we obtained cyclic peptides that bind to hepatocyte growth factor (HGF) or mesenchymal-epithelial transition factor. (MET) HGF-inhibitory peptide-8 (HiP-8) selectively bound to two-chain ... ...

Abstract	Using a random non-standard peptide integrated discovery system, we obtained cyclic peptides that bind to hepatocyte growth factor (HGF) or mesenchymal-epithelial transition factor. (MET) HGF-inhibitory peptide-8 (HiP-8) selectively bound to two-chain active HGF, but not to single-chain precursor HGF. HGF showed a dynamic change in its molecular shape in atomic force microscopy, but HiP-8 inhibited dynamic change in the molecular shape into a static status. The inhibition of the molecular dynamics of HGF by HiP-8 was associated with the loss of the ability to bind MET. HiP-8 could selectively detect active HGF in cancer tissues, and active HGF probed by HiP-8 showed co-localization with activated MET. Using HiP-8, cancer tissues with active HGF could be detected by positron emission tomography. HiP-8 seems to be applicable for the diagnosis and treatment of cancers. In contrast, based on the receptor dimerization as an essential process for activation, the cross-linking of the cyclic peptides that bind to the extracellular region of MET successfully generated an artificial ligand to MET. The synthetic MET agonists activated MET and exhibited biological activities which were indistinguishable from the effects of HGF. MET agonists composed of cyclic peptides can be manufactured by chemical synthesis but not recombinant protein expression, and thus are expected to be new biologics that are applicable to therapeutics and regenerative medicine.
MeSH term(s)	Animals ; Binding Sites ; Biological Products/pharmacology ; Biological Products/therapeutic use ; Gene Expression Regulation, Neoplastic/drug effects ; Hepatocyte Growth Factor/antagonists & inhibitors ; Hepatocyte Growth Factor/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Peptides, Cyclic/pharmacology ; Peptides, Cyclic/therapeutic use ; Protein Binding ; Proto-Oncogene Proteins c-met/agonists ; Proto-Oncogene Proteins c-met/chemistry ; Proto-Oncogene Proteins c-met/metabolism ; Signal Transduction/drug effects
Chemical Substances	Biological Products ; Peptides, Cyclic ; Hepatocyte Growth Factor (67256-21-7) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2020-10-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21217977
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Article ; Online: CDCP1 promotes compensatory renal growth by integrating Src and Met signaling.

Kajiwara, Kentaro / Yamano, Shotaro / Aoki, Kazuhiro / Okuzaki, Daisuke / Matsumoto, Kunio / Okada, Masato

Life science alliance

2021 Volume 4, Issue 4

Abstract: Compensatory growth of organs after loss of their mass and/or function is controlled by hepatocyte growth factor (HGF), but the underlying regulatory mechanisms remain elusive. Here, we show that CUB domain-containing protein 1 (CDCP1) promotes HGF- ... ...

Abstract	Compensatory growth of organs after loss of their mass and/or function is controlled by hepatocyte growth factor (HGF), but the underlying regulatory mechanisms remain elusive. Here, we show that CUB domain-containing protein 1 (CDCP1) promotes HGF-induced compensatory renal growth. Using canine kidney cells as a model of renal tubules, we found that HGF-induced temporal up-regulation of Src activity and its scaffold protein, CDCP1, and that the ablation of CDCP1 robustly abrogated HGF-induced phenotypic changes, such as morphological changes and cell growth/proliferation. Mechanistic analyses revealed that up-regulated CDCP1 recruits Src into lipid rafts to activate STAT3 associated with the HGF receptor Met, and activated STAT3 induces the expression of matrix metalloproteinases and mitogenic factors. After unilateral nephrectomy in mice, the Met-STAT3 signaling is transiently up-regulated in the renal tubules of the remaining kidney, whereas CDCP1 ablation attenuates regenerative signaling and significantly suppresses compensatory growth. These findings demonstrate that CDCP1 plays a crucial role in controlling compensatory renal growth by focally and temporally integrating Src and Met signaling.
MeSH term(s)	Animals ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/metabolism ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Cell Line ; Fluorescent Antibody Technique ; Hepatocyte Growth Factor/metabolism ; Humans ; Kidney/growth & development ; Kidney/metabolism ; Membrane Microdomains/metabolism ; Mice ; Mice, Knockout ; Phosphorylation ; Protein Binding ; Proto-Oncogene Proteins c-met/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; src-Family Kinases/metabolism
Chemical Substances	Antigens, Neoplasm ; CDCP1 protein, mouse ; Cell Adhesion Molecules ; STAT3 Transcription Factor ; Hepatocyte Growth Factor (67256-21-7) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2021-02-11
Publishing country	United States
Document type	Journal Article
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202000832
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Article: Placental Leucine Aminopeptidase as a Potential Specific Urine Biomarker for Invasive Ovarian Cancer.

Matsukawa, Tetsuya / Mizutani, Shigehiko / Matsumoto, Kunio / Kato, Yukio / Yoshihara, Masato / Kajiyama, Hiroaki / Shibata, Kiyosumi

Journal of clinical medicine

2021 Volume 11, Issue 1

Abstract: Background: A non-invasive and sensitive biomarker for the detection of ovarian cancer (OvCa) is lacking. We aim to investigate if urinary placental leucine aminopeptidase (P-LAP) can serve as a reliable biomarker for OvCa.: Methods: P-LAP activity ... ...

Abstract	Background: A non-invasive and sensitive biomarker for the detection of ovarian cancer (OvCa) is lacking. We aim to investigate if urinary placental leucine aminopeptidase (P-LAP) can serve as a reliable biomarker for OvCa. Methods: P-LAP activity was measured using a LAP assay kit (Serotech Co., Ltd., Sapporo, Japan) in the urine of 22 patients with benign or borderline malignant ovarian tumors and 18 patients with OvCa. In this assay, L-methionine was added at 20 mM because P-LAP is functional, but other aminopeptidases are inhibited at this dose of L-methionine. Results: The mean urinary P-LAP activity was significantly higher in the OvCa group than in the benign or borderline malignant tumor group. When the cut-off value of P-LAP was determined as 11.00 U/L, its sensitivity and specificity for differentiating invasive cancer were 77.8% and 95.5%, respectively. Conclusion: Although the usefulness of this test should be confirmed in a larger cohort of cases and controls, our study is the first to highlight the importance of urinary P-LAP as a biomarker for OvCa.
Language	English
Publishing date	2021-12-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm11010222
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