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Article ; Online: Vasculogenic mimicry: A dynamic event of malignancy.

Simizu, Siro

Biochimica et biophysica acta. General subjects

2022 Volume 1866, Issue 3, Page(s) 130084

MeSH term(s)	Neovascularization, Pathologic
Language	English
Publishing date	2022-01-06
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	60-7
ISSN	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2022.130084
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Article ; Online: ErbB4-mediated regulation of vasculogenic mimicry capability in breast cancer cells.

Kawahara, Ryota / Simizu, Siro

Cancer science

2022 Volume 113, Issue 3, Page(s) 950–959

Abstract: ErbB4 is a member of the ErbB receptor tyrosine kinase family. It has both pro- and anti-oncogenic activities in tumors. Vasculogenic mimicry (VM), a phenomenon in which cancer cells form capillary-like structures without endothelial cells, has been ... ...

Abstract	ErbB4 is a member of the ErbB receptor tyrosine kinase family. It has both pro- and anti-oncogenic activities in tumors. Vasculogenic mimicry (VM), a phenomenon in which cancer cells form capillary-like structures without endothelial cells, has been recognized to be a cause of malignant phenotypes in some solid tumors. Here, we used an in vitro VM formation assay, and demonstrated that ErbB4 negatively regulated VM formation in human breast cancer cells. By using CRISPR/Cas9-mediated gene knockout, we verified that the depletion of endogenous ErbB4 improved the VM formation capability. Although treatment with neuregulin 1 (NRG1), a ligand of ErbB4, induced the phosphorylation of ErbB4 and promoted VM formation in a dose-dependent manner, it did not induce such activities in kinase-dead K751M ErbB4-overexpressing cells. Moreover, we examined the effect of the missense mutation E872K of ErbB4, which has been reported in multiple tumors, on VM formation, and found that the mutation enhanced the basal phosphorylation level and ErbB4-mediated VM formation in the absence of NRG1 stimulation. Whereas NRG1 stimulated VM formation, excessive activation of ErbB4 induced a negative effect. In E872K ErbB4-overexpressing cells, but not in wild-type ErbB4-overexpressing cells, the number of VM tubes was significantly decreased by low-dose treatment with the ErbB inhibitor afatinib. Taken together, our findings demonstrated the significance of ErbB4-mediated VM formation, and suggested the possibility of ErbB4 mutations as effective targets in breast cancer.
MeSH term(s)	Afatinib/pharmacology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Female ; Humans ; Mutation ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Neuregulin-1/genetics ; Neuregulin-1/metabolism ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Receptor, ErbB-4/genetics ; Receptor, ErbB-4/metabolism
Chemical Substances	NRG1 protein, human ; Neuregulin-1 ; Protein Kinase Inhibitors ; Afatinib (41UD74L59M) ; ERBB4 protein, human (EC 2.7.10.1) ; Receptor, ErbB-4 (EC 2.7.10.1)
Language	English
Publishing date	2022-01-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1347-9032
ISSN (online)	1349-7006
ISSN	1347-9032
DOI	10.1111/cas.15258
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Article ; Online: Cofilin promotes vasculogenic mimicry by regulating the actin cytoskeleton in human breast cancer cells.

Nakajima, Minami / Kawahara, Ryota / Simizu, Siro

FEBS letters

2023 Volume 597, Issue 8, Page(s) 1114–1124

Abstract: Vasculogenic mimicry (VM) is the formation of microvascular channels by cancer cells. VM requires cellular processes that are regulated by changes in cellular migration and morphology. Cofilin (CFL), a key regulator of actin depolymerization, has been ... ...

Abstract	Vasculogenic mimicry (VM) is the formation of microvascular channels by cancer cells. VM requires cellular processes that are regulated by changes in cellular migration and morphology. Cofilin (CFL), a key regulator of actin depolymerization, has been reported to affect malignant phenotypes of cancer. We show that treatment with inhibitors of actin dynamics suppresses VM in MDA-MB-231 human breast cancer cells. We established CFL-knockout (KO) MDA-MB-231 cells and found that VM was attenuated in CFL-KO cells. Although the re-expression of wild-type CFL restored VM in CFL-KO cells, inactive phosphomimetic CFL failed to do so. Collectively, our results demonstrate that CFL is a critical regulator of VM and implicate CFL as a novel therapeutic target for breast cancer.
MeSH term(s)	Female ; Humans ; Actin Cytoskeleton ; Actin Depolymerizing Factors ; Actins ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Neovascularization, Pathologic/genetics
Chemical Substances	Actin Depolymerizing Factors ; Actins ; CFL1 protein, human
Language	English
Publishing date	2023-02-16
Publishing country	England
Document type	Journal Article
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.14594
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Article ; Online: Cofilin promotes vasculogenic mimicry by regulating the actin cytoskeleton in human breast cancer cells

Nakajima, Minami / Kawahara, Ryota / Simizu, Siro

FEBS Letters. 2023 Apr., v. 597, no. 8 p.1114-1124

2023

Abstract	Vasculogenic mimicry (VM) is the formation of microvascular channels by cancer cells. VM requires cellular processes that are regulated by changes in cellular migration and morphology. Cofilin (CFL), a key regulator of actin depolymerization, has been reported to affect malignant phenotypes of cancer. We show that treatment with inhibitors of actin dynamics suppresses VM in MDA‐MB‐231 human breast cancer cells. We established CFL‐knockout (KO) MDA‐MB‐231 cells and found that VM was attenuated in CFL‐KO cells. Although the re‐expression of wild‐type CFL restored VM in CFL‐KO cells, inactive phosphomimetic CFL failed to do so. Collectively, our results demonstrate that CFL is a critical regulator of VM and implicate CFL as a novel therapeutic target for breast cancer.
Keywords	actin ; breast neoplasms ; cell movement ; depolymerization ; humans ; microfilaments ; therapeutics
Language	English
Dates of publication	2023-04
Size	p. 1114-1124.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.14594
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Article ; Online: DPY19L3 promotes vasculogenic mimicry by its

Baydoun, Hassan / Kato, Yuji / Kamo, Hiroki / Hüsch, Anna / Mizuta, Hayato / Kawahara, Ryota / Simizu, Siro

Oncology research

2024 Volume 32, Issue 4, Page(s) 607–614

Abstract: ... ...

Abstract	C
MeSH term(s)	Female ; Humans ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Mannosyltransferases/genetics ; Mannosyltransferases/metabolism ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism
Chemical Substances	Mannosyltransferases (EC 2.4.1.-) ; DPY19L3 protein, human (EC 2.4.1.-)
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	1114699-0
ISSN	1555-3906 ; 0965-0407
ISSN (online)	1555-3906
ISSN	0965-0407
DOI	10.32604/or.2023.030304
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Article ; Online: Correction: Mori et al. Involvement of DPY19L3 in Myogenic Differentiation of C2C12 Myoblasts.

Mori, Kento / Sun, Hongkai / Miura, Kazuki / Simizu, Siro

Molecules (Basel, Switzerland)

2022 Volume 27, Issue 11

Abstract: In the original article [ ... ]. ...

Abstract	In the original article [...].
Language	English
Publishing date	2022-05-31
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27113534
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Article ; Online: Tyrosinase suppresses vasculogenic mimicry in human melanoma cells.

Kamo, Hiroki / Kawahara, Ryota / Simizu, Siro

Oncology letters

2022 Volume 23, Issue 5, Page(s) 169

Abstract: Melanoma is a type of skin cancer that derives from melanocytes; this tumor is highly metastatic and causes poor clinical outcomes in patients. Vasculogenic mimicry (VM), a vascular-like network that is formed by tumor cells instead of endothelial cells, ...

Abstract	Melanoma is a type of skin cancer that derives from melanocytes; this tumor is highly metastatic and causes poor clinical outcomes in patients. Vasculogenic mimicry (VM), a vascular-like network that is formed by tumor cells instead of endothelial cells, promotes the growth and metastasis of tumors by providing tumors with oxygen- and nutrient-containing blood. VM correlates with a poor prognosis in patients with melanoma, but the melanoma-specific mechanisms of VM are unknown. The present study revealed that treatment with the melanogenesis stimulators 3-isobutyl 1-methylxanthine (IBMX) and α-melanocyte-stimulating hormone (α-MSH) significantly inhibited VM in MNT-1 human pigmented melanoma cells. Tyrosinase (TYR), an essential enzyme in melanin production, was upregulated on treatment with α-MSH and IBMX, prompting an examination of the association between TYR and VM. A TYR inhibitor, arbutin, promoted VM in melanoma cells. Furthermore, CRISPR/Cas9-mediated knockout (KO) of TYR increased VM by melanoma cells. Notably, even in non-pigmented melanoma cells, TYR attenuated VM. Although re-expression of wild-type TYR suppressed VM in TYR-KO cells, T373K TYR, a frequently detected mutation in individuals with albinism, failed to inhibit VM. Overall, these results demonstrated that TYR negatively regulates VM, providing novel insights into the antioncogenic function of TYR in melanomas.
Language	English
Publishing date	2022-04-06
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2022.13289
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Article ; Online: C‐mannosylation regulates stabilization of RAMP1 protein and RAMP1‐mediated cell migration

Mizuta, Hayato / Takakusaki, Ayane / Suzuki, Takehiro / Otake, Keisuke / Dohmae, Naoshi / Simizu, Siro

The FEBS Journal. 2023 Jan., v. 290, no. 1 p.196-208

2023

Abstract: C‐mannosylation is a unique type of protein glycosylation via C‐C linkage between an α‐mannose and a tryptophan residue. This modification has been identified in about 30 proteins and regulates several functions, such as protein secretion and ... ...

Abstract	C‐mannosylation is a unique type of protein glycosylation via C‐C linkage between an α‐mannose and a tryptophan residue. This modification has been identified in about 30 proteins and regulates several functions, such as protein secretion and intracellular localization, as well as protein stability. About half of C‐mannosylated proteins are categorized as proteins containing thrombospondin type 1 repeat domain or type I cytokine receptors. To evaluate whether C‐mannosylation broadly affects protein functions regardless of protein domain or family, we have sought to identify other types of C‐mannosylated protein and analyse their functions. In this study, we focused on receptor activity modifying protein 1, which neither contains thrombospondin type 1 repeat domain nor belongs to the type I cytokine receptors. Our mass spectrometry analysis demonstrated that RAMP1 is C‐mannosylated at Trp⁵⁶. It has been shown that RAMP1 transports to the plasma membrane after dimerization with calcitonin receptor‐like receptor and is important for ligand‐dependent downstream signalling activation. Our results showed that C‐mannosylation has no effect on this transport activity. On the other hand, C‐mannosylation did enhance protein stability and cell migration activity. Our data may provide new insight into both C‐mannosylation research and novel RAMP1 analysis.
Keywords	calcitonin ; cell movement ; cytokines ; dimerization ; glycosylation ; mass spectrometry ; plasma membrane ; protein domains ; protein secretion ; tryptophan
Language	English
Dates of publication	2023-01
Size	p. 196-208.
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16592
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Article ; Online: Destabilization of vitelline membrane outer layer protein 1 homolog (VMO1) by C‐mannosylation

Yoshimoto, Satoshi / Suzuki, Takehiro / Ōtani, Naoki / Takahashi, Daisuke / Toshima, Kazunobu / Dohmae, Naoshi / Simizu, Siro

FEBS Open Bio 2023 Mar., v. 13, no. 3, p. 490-499

2023 , Page(s) 490–499

Abstract: C‐mannosylation is a rare type of protein glycosylation whereby a single mannose is added to the first tryptophan in the consensus sequence Trp‐Xaa‐Xaa‐Trp/Cys (in which Xaa represents any amino acid). Its consensus sequence is mainly found in proteins ... ...

Abstract	C‐mannosylation is a rare type of protein glycosylation whereby a single mannose is added to the first tryptophan in the consensus sequence Trp‐Xaa‐Xaa‐Trp/Cys (in which Xaa represents any amino acid). Its consensus sequence is mainly found in proteins containing a thrombospondin type‐1 repeat (TSR1) domain and in type I cytokine receptors. In these proteins, C‐mannosylation affects protein secretion, intracellular localization, and protein stability; however, the role of C‐mannosylation in proteins that are not type I cytokine receptors and/or do not contain a TSR1 domain is less well explored. In this study, we focused on human vitelline membrane outer layer protein 1 homolog (VMO1). VMO1, which possesses two putative C‐mannosylation sites, is a 21‐kDa secreted protein that does not contain a TSR1 domain and is not a type I cytokine receptor. Mass spectrometry analyses revealed that VMO1 is C‐mannosylated at Trp¹⁰⁵ but not at Trp⁴⁴. Although C‐mannosylation does not affect the extracellular secretion of VMO1, it destabilizes the intracellular VMO1. In addition, a structural comparison between VMO1 and C‐mannosylated VMO1 showed that the modification of the mannose changes the conformation of three loops in VMO1. Taken together, our results demonstrate the first example of C‐mannosylation for protein destabilization of VMO1.
Keywords	consensus sequence ; cytokine receptors ; cytokines ; glycosylation ; humans ; mannose ; mass spectrometry ; protein secretion ; tryptophan ; vitelline membrane
Language	English
Dates of publication	2023-03
Size	p. 490-499
Publishing place	John Wiley & Sons, Ltd
Document type	Article ; Online
Note	JOURNAL ARTICLE
ZDB-ID	2651702-4
ISSN	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13561
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Article ; Online: Destabilization of vitelline membrane outer layer protein 1 homolog (VMO1) by C-mannosylation.

Yoshimoto, Satoshi / Suzuki, Takehiro / Otani, Naoki / Takahashi, Daisuke / Toshima, Kazunobu / Dohmae, Naoshi / Simizu, Siro

FEBS open bio

2023 Volume 13, Issue 3, Page(s) 490–499

Abstract: C-mannosylation is a rare type of protein glycosylation whereby a single mannose is added to the first tryptophan in the consensus sequence Trp-Xaa-Xaa-Trp/Cys (in which Xaa represents any amino acid). Its consensus sequence is mainly found in proteins ... ...

Abstract	C-mannosylation is a rare type of protein glycosylation whereby a single mannose is added to the first tryptophan in the consensus sequence Trp-Xaa-Xaa-Trp/Cys (in which Xaa represents any amino acid). Its consensus sequence is mainly found in proteins containing a thrombospondin type-1 repeat (TSR1) domain and in type I cytokine receptors. In these proteins, C-mannosylation affects protein secretion, intracellular localization, and protein stability; however, the role of C-mannosylation in proteins that are not type I cytokine receptors and/or do not contain a TSR1 domain is less well explored. In this study, we focused on human vitelline membrane outer layer protein 1 homolog (VMO1). VMO1, which possesses two putative C-mannosylation sites, is a 21-kDa secreted protein that does not contain a TSR1 domain and is not a type I cytokine receptor. Mass spectrometry analyses revealed that VMO1 is C-mannosylated at Trp
MeSH term(s)	Humans ; Glycosylation ; Mannose/metabolism ; Vitelline Membrane/metabolism ; Protein Transport ; Receptors, Cytokine/metabolism
Chemical Substances	Mannose (PHA4727WTP) ; Receptors, Cytokine
Language	English
Publishing date	2023-01-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2651702-4
ISSN	2211-5463 ; 2211-5463
ISSN (online)	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13561
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