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Article: Immaturin-Nuclease as a Model System for a Gene-Programmed Sexual Development and Rejuvenescence in

Haga, Nobuyuki / Usui, Toshinori / Takenaka, Yasuhiro / Chiba, Yuta / Abe, Tomoaki

2022 Volume 11, Issue 1

Abstract: Fertilization-initiated development and adult-onset aging are standard features in the life history of eukaryotes. ... ...

Abstract	Fertilization-initiated development and adult-onset aging are standard features in the life history of eukaryotes. In
Language	English
Publishing date	2022-12-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms11010082
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Article ; Online: La-Related Protein 4 as a Suppressor for Motility of Ovarian Cancer Cells.

Egiz, Mahy / Usui, Toshinori / Ishibashi, Masumi / Zhang, Xuewei / Shigeta, Shogo / Toyoshima, Masafumi / Kitatani, Kazuyuki / Yaegashi, Nobuo

The Tohoku journal of experimental medicine

2019 Volume 247, Issue 1, Page(s) 59–67

Abstract: The La-related proteins (LARPs) are a family of RNA binding proteins that control the degradation and stabilization of RNAs. As emerging research reveals the biology of each LARP, it is evident that LARPs are dysregulated in some types of cancer. ... ...

Abstract	The La-related proteins (LARPs) are a family of RNA binding proteins that control the degradation and stabilization of RNAs. As emerging research reveals the biology of each LARP, it is evident that LARPs are dysregulated in some types of cancer. Upregulation of cell motility potentiates the metastatic potential of ovarian cancer cells; however, the roles of LARPs in cell motility remain unknown. In the present study, we investigated the roles of LARPs in the progression of ovarian cancer using SKOV3 human ovarian cancer cells and a public database that integrates microarray-based gene expression data and clinical data. To explore the involvement of LARPs in the cell motility, we performed RNA interference screening for LARP mRNAs in SKOV3 cells. The screening identified LARP4 as a potential suppressor of the formation of lamellipodia. Conversely, enforced expression of LARP4 suppressed the formation of lamellipodia. Moreover, cell migration was significantly increased in LARP4-depleted SKOV3 cells. Mechanistically, LARP4 depletion was associated with the decrease in RhoA protein expression. These results suggest that LARP4 may limit RhoA-dependent cell motility. In a mouse xenograft model with SKOV3 cells, LARP4 depletion potentiated peritoneal metastasis. Upon analysis of a public database of patients with ovarian cancer, the LARP4 mRNA-high expression group (n = 166) showed longer overall survival compared with the LARP4 mRNA-low expression group (n = 489), implying a positive correlation of LARP4 mRNA levels in ovarian cancer tissues with patient prognosis. Taken together, we propose that LARP4 could suppress motility and metastatic potential of ovarian cancer cells.
MeSH term(s)	Animals ; Autoantigens/genetics ; Autoantigens/metabolism ; Cell Line, Tumor ; Cell Movement ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Metastasis ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; Ovarian Neoplasms/pathology ; Pseudopodia/metabolism ; Ribonucleoproteins/genetics ; Ribonucleoproteins/metabolism ; Survival Analysis ; Xenograft Model Antitumor Assays ; rhoA GTP-Binding Protein/metabolism ; SS-B Antigen
Chemical Substances	Autoantigens ; Ribonucleoproteins ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2019-02-11
Publishing country	Japan
Document type	Journal Article
ZDB-ID	123477-8
ISSN	1349-3329 ; 0040-8727
ISSN (online)	1349-3329
ISSN	0040-8727
DOI	10.1620/tjem.247.59
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Article ; Online: Understanding the glass-forming ability of active pharmaceutical ingredients for designing supersaturating dosage forms.

Kawakami, Kohsaku / Usui, Toshinori / Hattori, Mitsunari

Journal of pharmaceutical sciences

2012 Volume 101, Issue 9, Page(s) 3239–3248

Abstract: Amorphous solid dispersions have great potential for enhancing oral absorption of poorly soluble drugs. Crystallization behavior during storage and after exposure to aqueous media must be examined in detail for designing stable and effective amorphous ... ...

Abstract	Amorphous solid dispersions have great potential for enhancing oral absorption of poorly soluble drugs. Crystallization behavior during storage and after exposure to aqueous media must be examined in detail for designing stable and effective amorphous formulations, and it is significantly affected by the intrinsic properties of an amorphous drug. Many attempts have been made to correlate various thermodynamic parameters of pharmaceutical glasses with their crystallization behavior; however, variations in model drugs that could be used for such investigation has been limited because the amorphous characteristics of drugs possessing a high crystallization tendency are difficult to evaluate. In this study, high-speed differential scanning calorimetry, which could inhibit their crystallization using high cooling rates up to 2000°C/s, was employed for assessing such drugs. The thermodynamic parameters of the glasses, including glass transition temperature (T(g)) and fragility, were obtained to show that their crystallization tendency cannot be explained simply by the parameters, although there have been general thought that fragility may be correlated with crystallization tendency. Also investigated was correlation between the thermodynamic parameters and crystallization tendency upon contact with water, which influences in vivo efficacy of amorphous formulations. T(g) was correlated well with the crystallization tendency upon contact with water.
MeSH term(s)	Calorimetry, Differential Scanning ; Chemistry, Pharmaceutical ; Crystallization ; Dosage Forms ; Drug Stability ; Hydrogen Bonding ; Models, Chemical ; Pharmaceutical Preparations/chemistry ; Solvents/chemistry ; Technology, Pharmaceutical/methods ; Transition Temperature ; Water/chemistry
Chemical Substances	Dosage Forms ; Pharmaceutical Preparations ; Solvents ; Water (059QF0KO0R)
Language	English
Publishing date	2012-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3151-3
ISSN	1520-6017 ; 0022-3549
ISSN (online)	1520-6017
ISSN	0022-3549
DOI	10.1002/jps.23166
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Article ; Online: Tyrosine kinase receptor TIE-1 mediates platinum resistance by promoting nucleotide excision repair in ovarian cancer.

Ishibashi, Masumi / Toyoshima, Masafumi / Zhang, Xuewei / Hasegawa-Minato, Junko / Shigeta, Shogo / Usui, Toshinori / Kemp, Christopher J / Grandori, Carla / Kitatani, Kazuyuki / Yaegashi, Nobuo

Scientific reports

2018 Volume 8, Issue 1, Page(s) 13207

Abstract: Platinum resistance is one of the most challenging problems in ovarian cancer treatment. High-throughput functional siRNA screening identified tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (TIE-1) as a gene that confers cells resistant ... ...

Abstract	Platinum resistance is one of the most challenging problems in ovarian cancer treatment. High-throughput functional siRNA screening identified tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (TIE-1) as a gene that confers cells resistant to cisplatin. Conversely enforced over-expression of TIE-1 was validated to decrease cisplatin sensitivity in multiple ovarian cancer cell lines and up-regulation of TIE-1 was correlated with poor prognosis and cisplatin resistance in patients with ovarian cancer. Mechanistically, TIE-1 up-regulates the nucleotide excision repair (NER) system mediated by xeroderma pigmentosum complementation group C (XPC), thereby leading to decreased susceptibility to cisplatin-induced cell death without affecting cisplatin uptake and excretion. Importantly potentiation of therapeutic efficacy by TIE-1 inhibition was selective to DNA-adduct-type chemotherapeutic platinum reagents. Therefore, TIE-1 is suggested to promote XPC-dependent NER, rendering ovarian cancer cells resistant to platinum. Accompanied with novel findings, TIE-1 could represent as a novel therapeutic target for platinum-resistant ovarian cancer.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; DNA Repair/drug effects ; Drug Resistance, Neoplasm ; Female ; Humans ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; Receptor, TIE-1/metabolism
Chemical Substances	Antineoplastic Agents ; Receptor, TIE-1 (EC 2.7.10.1) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2018-09-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-31069-2
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Article ; Online: Activation of p38 Mitogen-Activated Protein Kinase in Gaucher's Disease.

Kitatani, Kazuyuki / Wada, Masayuki / Perry, David / Usui, Toshinori / Sun, Ying / Obeid, Lina M / Yaegashi, Nobuo / Grabowski, Gregory A / Hannun, Yusuf A

PloS one

2015 Volume 10, Issue 8, Page(s) e0136633

Abstract: Gaucher's disease is caused by defects in acid β-glucosidase 1 (GBA1) and has been also proposed as an inflammatory disease. GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation ...

Abstract	Gaucher's disease is caused by defects in acid β-glucosidase 1 (GBA1) and has been also proposed as an inflammatory disease. GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation in glucosylceramide and insufficient formation of ceramide. We investigated if the pro-inflammatory kinase p38 is activated in Gaucher's disease, since ceramide has been proposed to suppress p38 activation. Three Gaucher's disease mouse models were employed, and p38 was found to be activated in lung and liver tissues of all Gaucher's disease mice. Most interestingly, neuronopathic Gaucher's disease type mice, but not non-neuronopathic ones, displayed significant activation of p38 and up-regulation of p38-inducible proinflammatory cytokines in brain tissues. In addition, all type of Gaucher's disease mice also showed increases in serum IL-6. As cellular signalling is believed to represent an in vivo inflammatory phenotype in Gaucher's disease, activation of p38 and possibly its-associated formation of proinflammatory cytokines were assessed in fibroblasts established from neuronopathic Gaucher's disease mice. In mouse Gaucher's disease cells, p38 activation and IL-6 formation by TNF-α treatment were enhanced as compared to those of wild type. Furthermore, human fibroblasts from Gaucher's disease patients also displayed increases in p38 activation and IL-6 formation as comparison to healthy counterpart. These results raise the potential that proinflammatory responses such as p38 activation and IL-6 formation are augmented in Gaucher's disease.
MeSH term(s)	Animals ; Cell Line ; Disease Models, Animal ; Enzyme Activation/genetics ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gaucher Disease/enzymology ; Gaucher Disease/genetics ; Gaucher Disease/pathology ; Gene Expression Regulation, Enzymologic ; Glucosylceramidase/genetics ; Glucosylceramidase/metabolism ; Glucosylceramides/genetics ; Glucosylceramides/metabolism ; Humans ; Interleukin-6/biosynthesis ; Interleukin-6/genetics ; Mice ; Mice, Mutant Strains ; Up-Regulation ; p38 Mitogen-Activated Protein Kinases/biosynthesis ; p38 Mitogen-Activated Protein Kinases/genetics
Chemical Substances	Glucosylceramides ; IL6 protein, human ; Interleukin-6 ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Glucosylceramidase (EC 3.2.1.45)
Language	English
Publishing date	2015-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0136633
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Article ; Online: Ceramide Nanoliposomes as a MLKL-Dependent, Necroptosis-Inducing, Chemotherapeutic Reagent in Ovarian Cancer.

Zhang, Xuewei / Kitatani, Kazuyuki / Toyoshima, Masafumi / Ishibashi, Masumi / Usui, Toshinori / Minato, Junko / Egiz, Mahy / Shigeta, Shogo / Fox, Todd / Deering, Tye / Kester, Mark / Yaegashi, Nobuo

Molecular cancer therapeutics

2017 Volume 17, Issue 1, Page(s) 50–59

Abstract: Ceramides are bioactive lipids that mediate cell death in cancer cells, and ceramide-based therapy is now being tested in dose-escalating phase I clinical trials as a cancer treatment. Multiple nanoscale delivery systems for ceramide have been proposed ... ...

Abstract	Ceramides are bioactive lipids that mediate cell death in cancer cells, and ceramide-based therapy is now being tested in dose-escalating phase I clinical trials as a cancer treatment. Multiple nanoscale delivery systems for ceramide have been proposed to overcome the inherent toxicities, poor pharmacokinetics, and difficult biophysics associated with ceramide. Using the ceramide nanoliposomes (CNL), we now investigate the therapeutic efficacy and signaling mechanisms of this nanoscale delivery platform in refractory ovarian cancer. Treatment of ovarian cancer cells with CNL decreased the number of living cells through necroptosis but not apoptosis. Mechanistically, dying SKOV3 ovarian cancer cells exhibit activation of pseudokinase mixed lineage kinase domain-like (MLKL) as evidenced by oligomerization and relocalization to the blebbing membranes, showing necroptotic characteristics. Knockdown of MLKL, but not its upstream protein kinases such as receptor-interacting protein kinases, with siRNA significantly abolished CNL-induced cell death. Monomeric MLKL protein expression inversely correlated with the IC
MeSH term(s)	Apoptosis ; Ceramides/metabolism ; Female ; Humans ; Necrosis ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Protein Kinases/genetics ; Transfection
Chemical Substances	Ceramides ; MLKL protein, human (EC 2.7.-) ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2017-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-17-0173
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Article ; Online: Inhibition of plasminogen activator inhibitor-1 is a potential therapeutic strategy in ovarian cancer.

Mashiko, Satsuki / Kitatani, Kazuyuki / Toyoshima, Masafumi / Ichimura, Atsuhiko / Dan, Takashi / Usui, Toshinori / Ishibashi, Masumi / Shigeta, Shogo / Nagase, Satoru / Miyata, Toshio / Yaegashi, Nobuo

Cancer biology & therapy

2014 Volume 16, Issue 2, Page(s) 253–260

Abstract: Plasminogen activator inhibitor (PAI)-1 is predictive of poor outcome in several types of cancer. The present study investigated the biological role for PAI-1 in ovarian cancer and potential of targeted pharmacotherapeutics. In patients with ovarian ... ...

Abstract	Plasminogen activator inhibitor (PAI)-1 is predictive of poor outcome in several types of cancer. The present study investigated the biological role for PAI-1 in ovarian cancer and potential of targeted pharmacotherapeutics. In patients with ovarian cancer, PAI-1 mRNA expression in tumor tissues was positively correlated with poor prognosis. To determine the role of PAI-1 in cell proliferation in ovarian cancer, the effects of PAI-1 inhibition were examined in PAI-1-expressing ovarian cancer cells. PAI-1 knockdown by small interfering RNA resulted in significant suppression of cell growth accompanied with G2/M cell cycle arrest and intrinsic apoptosis. Similarly, treatment with the small molecule PAI-1 inhibitor TM5275 effectively blocked cell proliferation of ovarian cancer cells that highly express PAI-1. Together these results suggest that PAI-1 promotes cell growth in ovarian cancer. Interestingly, expression of PAI-1 was increased in ovarian clear cell carcinoma compared with that in serous tumors. Our results suggest that PAI-1 inhibition promotes cell cycle arrest and apoptosis in ovarian cancer and that PAI-1 inhibitors potentially represent a novel class of anti-tumor agents.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Immunohistochemistry ; Inhibitory Concentration 50 ; Molecular Targeted Therapy ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; Ovarian Neoplasms/mortality ; Ovarian Neoplasms/pathology ; Piperazines/pharmacology ; Plasminogen Activator Inhibitor 1/genetics ; Plasminogen Activator Inhibitor 1/metabolism ; Plasminogen Inactivators/pharmacology ; Prognosis ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Up-Regulation ; para-Aminobenzoates/pharmacology
Chemical Substances	5-chloro-2-(((2-(4-(diphenylmethyl)piperazin-1-yl)-2-oxoethoxy)acetyl)amino)benzoate ; Antineoplastic Agents ; Piperazines ; Plasminogen Activator Inhibitor 1 ; Plasminogen Inactivators ; RNA, Messenger ; RNA, Small Interfering ; para-Aminobenzoates
Language	English
Publishing date	2014-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.1080/15384047.2014.1001271
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Zs.A 5887: Show issues

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Article: Kinetic study of thermal Z to E isomerization reactions of azobenzene and 4-dimethylamino-4'-nitroazobenzene in ionic liquids [1-R-3-methylimidazolium bis(trifluoromethylsulfonyl)imide with R = butyl, pentyl, and hexyl].

Baba, Keita / Ono, Hajime / Itoh, Eri / Itoh, Sumitaka / Noda, Kyoko / Usui, Toshinori / Ishihara, Koji / Inamo, Masahiko / Takagi, Hideo D / Asano, Tsutomu

Chemistry (Weinheim an der Bergstrasse, Germany)

2006 Volume 12, Issue 20, Page(s) 5328–5333

Abstract: Thermal Z to E isomerization reactions of azobenzene and 4-dimethylamino-4'-nitroazobenzene were examined in three ionic liquids of general formula 1-R-3-methylimidazolium bis(trifluoromethylsulfonyl)imide (R = butyl, pentyl, and hexyl). The first-order ... ...

Abstract	Thermal Z to E isomerization reactions of azobenzene and 4-dimethylamino-4'-nitroazobenzene were examined in three ionic liquids of general formula 1-R-3-methylimidazolium bis(trifluoromethylsulfonyl)imide (R = butyl, pentyl, and hexyl). The first-order rate constants and activation energies for the reactions of azobenzene measured in these ionic liquids were consistent with those measured in ordinary organic solvents, which indicated that the slow isomerization through the inversion mechanism with a nonpolar transition state was little influenced by the solvent properties, such as the viscosity and dielectric constant, of ionic liquids. On the other hand, the rate constants and the corresponding frequency factors of the Arrhenius plot were significantly reduced for the isomerization of 4-dimethylamino-4'-nitroazobenzene in ionic liquids compared with those for the isomerization in ordinary organic molecular solvents with similar dielectric properties. Although these ionic liquids are viscous, the apparent viscosity dependence of the rate constant could not be explained either by the Kramers-Grote-Hynes model or by the Agmon-Hopfield model for solution reactions. It is proposed that the positive and the negative charge centers of a highly polar rotational transition state are stabilized by the surrounding anions and cations, respectively, and that the ions must be rearranged so as to form highly ordered solvation shells around the charge centers of the reactant in the transition state. This requirement for the orderly solvation in the transition state results in unusually small frequency factors of 10(4)-10(7) s(-1).
Language	English
Publishing date	2006-07-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1478547-x
ISSN	1521-3765 ; 0947-6539
ISSN (online)	1521-3765
ISSN	0947-6539
DOI	10.1002/chem.200600081
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Article: Immaturin-Nuclease as a Model System for a Gene-Programmed Sexual Development and Rejuvenescence in

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Article ; Online: La-Related Protein 4 as a Suppressor for Motility of Ovarian Cancer Cells.

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Article ; Online: Understanding the glass-forming ability of active pharmaceutical ingredients for designing supersaturating dosage forms.

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Article ; Online: Tyrosine kinase receptor TIE-1 mediates platinum resistance by promoting nucleotide excision repair in ovarian cancer.

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Article ; Online: Activation of p38 Mitogen-Activated Protein Kinase in Gaucher's Disease.

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Article ; Online: Ceramide Nanoliposomes as a MLKL-Dependent, Necroptosis-Inducing, Chemotherapeutic Reagent in Ovarian Cancer.

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Article ; Online: Inhibition of plasminogen activator inhibitor-1 is a potential therapeutic strategy in ovarian cancer.

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Article: Kinetic study of thermal Z to E isomerization reactions of azobenzene and 4-dimethylamino-4'-nitroazobenzene in ionic liquids [1-R-3-methylimidazolium bis(trifluoromethylsulfonyl)imide with R = butyl, pentyl, and hexyl].

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