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Article ; Online: Unilateral atrophy of the masticatory muscles and mandibular ramus due to pure trigeminal motor neuropathy: a case report.

Chiba, Masatoshi / Echigo, Seishi

Oral surgery, oral medicine, oral pathology and oral radiology

2012 Volume 113, Issue 6, Page(s) e30–4

Abstract: Pure trigeminal motor neuropathy is a very unusual disease that is characterized by trigeminal motor paralysis without trigeminal sensory disturbances and without the involvement of the other cranial nerves. We report a case of pure trigeminal motor ... ...

Abstract	Pure trigeminal motor neuropathy is a very unusual disease that is characterized by trigeminal motor paralysis without trigeminal sensory disturbances and without the involvement of the other cranial nerves. We report a case of pure trigeminal motor neuropathy in a 70-year-old woman. The diagnosis was based on the results of clinical, electromyographic, and radiologic examinations. Only the motor branch of the left trigeminal nerve was damaged. Atrophy of the left-side masticatory muscles and jaw resulted in facial asymmetry. Magnetic resonance imaging (MRI) of the head and face did not detect any pathologic lesion, with the exception of atrophy and fatty infiltration of the muscles innervated by the left trigeminal motor nerve. The etiology of the patient's pure trigeminal motor neuropathy was undetermined. Patients with suspected trigeminal motor neuropathy should undergo MRI of the head and face to evaluate the sequelae of denervation and to detect an intracranial or extracranial lesion.
MeSH term(s)	Aged ; Electromyography ; Facial Asymmetry/etiology ; Female ; Humans ; Mandible/pathology ; Masticatory Muscles/pathology ; Motor Neuron Disease/complications ; Muscular Atrophy/etiology ; Trigeminal Nerve Diseases/complications
Language	English
Publishing date	2012-06
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2650843-6
ISSN	2212-4411 ; 2212-4403
ISSN (online)	2212-4411
ISSN	2212-4403
DOI	10.1016/j.oooo.2011.11.022
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Article ; Online: Glucose and glutamine metabolism in oral squamous cell carcinoma: insight from a quantitative metabolomic approach.

Ogawa, Tamaki / Washio, Jumpei / Takahashi, Tetsu / Echigo, Seishi / Takahashi, Nobuhiro

Oral surgery, oral medicine, oral pathology and oral radiology

2014 Volume 118, Issue 2, Page(s) 218–225

Abstract: Objective: To characterize the metabolic system of oral squamous cell carcinoma (OSCC) by metabolome analysis.: Study design: The metabolome profiles, including the Embden-Meyerhof-Parnas pathway (EMPP), the pentose phosphate pathway, the ... ...

Abstract	Objective: To characterize the metabolic system of oral squamous cell carcinoma (OSCC) by metabolome analysis. Study design: The metabolome profiles, including the Embden-Meyerhof-Parnas pathway (EMPP), the pentose phosphate pathway, the tricarboxylic acid cycle (TCAC), and amino acids, were obtained from OSCC and its surrounding normal tissues (32 patients) using capillary electrophoresis and a time-of-flight mass spectrometer. Results: Enhancement of glucose consumption and lactate production (Warburg effect) was observed in OSCC tissues. The decrease of glucose along with the decrease of the downstream intermediates in the EMPP suggests that incorporated glucose is mainly consumed for biosynthesis. Glutamine consumption with the increase of the intermediates in the last half of the TCAC suggests the involvement of glutaminolysis, in which glutamine is converted to lactate via the last half of the TCAC. Conclusions: It is suggested that OSCC tissues show the Warburg effect, which stems from the combined enhancement of glucose consumption and glutaminolysis.
MeSH term(s)	Aged ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/pathology ; Electrophoresis, Capillary ; Female ; Glucose/metabolism ; Glutamine/metabolism ; Humans ; Male ; Metabolomics ; Mouth Neoplasms/metabolism ; Mouth Neoplasms/pathology ; Neoplasm Staging ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Chemical Substances	Glutamine (0RH81L854J) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2014-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2650843-6
ISSN	2212-4411 ; 2212-4403
ISSN (online)	2212-4411
ISSN	2212-4403
DOI	10.1016/j.oooo.2014.04.003
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Article ; Online: Involvement of sensory neurons in bone defect repair in rats.

Henmi, Akiko / Nakamura, Megumi / Echigo, Seishi / Sasano, Yasuyuki

Journal of electron microscopy

2011 Volume 60, Issue 6, Page(s) 393–400

Abstract: We investigated bone repair in sensory-denervated rats, compared with controls, to elucidate the involvement of sensory neurons. Nine-week-old male Wistar rats received subcutaneous injections of capsaicin to denervate sensory neurons. Rats treated with ... ...

Abstract	We investigated bone repair in sensory-denervated rats, compared with controls, to elucidate the involvement of sensory neurons. Nine-week-old male Wistar rats received subcutaneous injections of capsaicin to denervate sensory neurons. Rats treated with the same amount of vehicle served as controls. A standardized bone defect was created on the parietal bone. We measured the amount of repaired bone with quantitative radiographic analysis and the mRNA expressions of osteocalcin and cathepsin K with real-time polymerase chain reaction (PCR). Quantitative radiographic analysis showed that the standard deviations and coefficients of variation for the amount of repaired bone were much higher in the capsaicin-treated group than in the control group at any time point, which means that larger individual differences in the amount of repaired bone were found in capsaicin-treated rats than controls. Furthermore, radiographs showed radiolucency in pre-existing bone surrounding the standardized defect only in the capsaicin-treated group, and histological observation demonstrated some multinuclear cells corresponding to the radiolucent area. Real-time PCR indicated that there was no significant difference in the mRNA expression levels of osteocalcin and cathepsin K between the control group and the capsaicin-treated group. These results suggest that capsaicin-induced sensory denervation affects the bone defect repair.
MeSH term(s)	Animals ; Biomarkers ; Bone Regeneration ; Capsaicin/administration & dosage ; Cathepsin K/genetics ; Cathepsin K/metabolism ; Gene Expression Regulation ; Injections, Subcutaneous ; Male ; Osteocalcin/genetics ; Osteocalcin/metabolism ; Osteoclasts/metabolism ; Osteoclasts/pathology ; Parietal Bone/diagnostic imaging ; Parietal Bone/drug effects ; Parietal Bone/injuries ; Parietal Bone/pathology ; RNA, Messenger/genetics ; RNA, Messenger/isolation & purification ; RNA, Messenger/metabolism ; Radiography ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Sensory Receptor Cells/drug effects ; Sensory Receptor Cells/pathology
Chemical Substances	Biomarkers ; RNA, Messenger ; Osteocalcin (104982-03-8) ; Cathepsin K (EC 3.4.22.38) ; Capsaicin (S07O44R1ZM)
Language	English
Publishing date	2011-12
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1029601-3
ISSN	1477-9986 ; 0022-0744
ISSN (online)	1477-9986
ISSN	0022-0744
DOI	10.1093/jmicro/dfr075
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Zs.B 1211: Show issues

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Article ; Online: Osteochondroma of the mandibular condyle manifesting only as conductive hearing loss.

Hidaka, Hiroshi / Kobayashi, Toshimitsu / Ishida, Kazuyuki / Echigo, Seishi

Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery

2010 Volume 143, Issue 5, Page(s) 710–711

MeSH term(s)	Audiometry ; Diagnosis, Differential ; Follow-Up Studies ; Hearing Loss, Conductive/diagnosis ; Hearing Loss, Conductive/etiology ; Hearing Loss, Conductive/surgery ; Humans ; Male ; Mandibular Condyle ; Mandibular Neoplasms/complications ; Mandibular Neoplasms/diagnosis ; Mandibular Neoplasms/surgery ; Middle Aged ; Oral Surgical Procedures/methods ; Osteochondroma/complications ; Osteochondroma/diagnosis ; Osteochondroma/surgery ; Tomography, X-Ray Computed
Language	English
Publishing date	2010-11
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	392085-9
ISSN	1097-6817 ; 0161-6439 ; 0194-5998
ISSN (online)	1097-6817
ISSN	0161-6439 ; 0194-5998
DOI	10.1016/j.otohns.2010.08.004
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Article ; Online: First clinical application of octacalcium phosphate collagen composite in human bone defect.

Kawai, Tadashi / Echigo, Seishi / Matsui, Keiko / Tanuma, Yuji / Takahashi, Tetsu / Suzuki, Osamu / Kamakura, Shinji

Tissue engineering. Part A

2014 Volume 20, Issue 7-8, Page(s) 1336–1341

Abstract: We have previously demonstrated that octacalcium phosphate (OCP) collagen composite (OCP/collagen) promotes bone regeneration in a critical-sized bone defect of a rodent or canine model. This study was designed to investigate the bone regeneration of OCP/ ...

Abstract	We have previously demonstrated that octacalcium phosphate (OCP) collagen composite (OCP/collagen) promotes bone regeneration in a critical-sized bone defect of a rodent or canine model. This study was designed to investigate the bone regeneration of OCP/collagen in human bone defect as a first clinical trial. Two patients who had a radicular cyst or apical periodontitis consented to participate in our clinical study, and OCP/collagen was implanted into the defects after operation. Radiographic examination showed effective bone healing in each bone defect at 3 or 6 months. Likewise, computed tomography value significantly increased after implantation. Postoperative wound healing was uneventful, and neither infection nor allergic reaction against OCP/collagen was observed for the entire period. This study demonstrated that OCP/collagen would be safely used and enhanced bone regeneration in human bone defects. To reinforce the efficacy of OCP/collagen as a bone substitute material, it should be compared with other suitable comparators in the future.
MeSH term(s)	Adult ; Bone and Bones/diagnostic imaging ; Bone and Bones/drug effects ; Bone and Bones/pathology ; Bone and Bones/surgery ; Calcium Phosphates/pharmacology ; Collagen/pharmacology ; Female ; Humans ; Male ; Prosthesis Implantation ; Tissue Scaffolds/chemistry ; Tomography, X-Ray Computed ; Young Adult
Chemical Substances	Calcium Phosphates ; octacalcium phosphate (13767-12-9) ; Collagen (9007-34-5)
Language	English
Publishing date	2014-01-16
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2420582-5
ISSN	1937-335X ; 1937-3341
ISSN (online)	1937-335X
ISSN	1937-3341
DOI	10.1089/ten.TEA.2013.0508
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Zs.A 5500/A: Show issues

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Article ; Online: Immunohistochemical assessment of ATG7, LC3, and p62 in ameloblastomas.

Okada, Miwa / Oikawa, Mariko / Miki, Yasuhiro / Shimizu, Yoshinaka / Echigo, Seishi / Takahashi, Tetsu / Kumamoto, Hiroyuki

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology

2014 Volume 43, Issue 8, Page(s) 606–612

Abstract: Background: To investigate the roles of autophagy in tumorigenesis, cytodifferentiation, and prognosis of odontogenic tumors, we analyzed the immunohistochemical expression of ATG7, LC3, and p62 in odontogenic tissues.: Methods: Tissue specimens of ... ...

Abstract	Background: To investigate the roles of autophagy in tumorigenesis, cytodifferentiation, and prognosis of odontogenic tumors, we analyzed the immunohistochemical expression of ATG7, LC3, and p62 in odontogenic tissues. Methods: Tissue specimens of nine dental follicles and 69 ameloblastomas were immunohistochemically examined with antibodies against ATG7, LC3, and p62. Results: Immunohistochemical reactivity for ATG7, LC3, and p62 was detected in many odontogenic epithelial cells and several endothelial cells and fibroblasts in dental follicles and ameloblastomas. ATG7 reactivity in ameloblatomas was significantly higher than that in dental follicles. Expression of ATG7, LC3, and p62 was found markedly in neoplastic cells near the basement membrane rather than central polyhedral cells in ameloblastomas. Reactivity for these molecules was significantly higher in unicystic ameloblastomas than in solid ameloblastomas. Granular cells in granular cell ameloblastomas showed obvious reactivity for the autophagy- related molecules, and LC3 reactivity in granular cell ameloblastomas was significantly higher than in other ameloblastoma variations. Recurrent ameloblastomas showed significantly lower reactivity of LC3 and p62 than primary ameloblastomas. Conclusions: Expression of ATG7, LC3, and p62 in dental follicles and ameloblastomas suggests that autophagy regulation might be affected by microenvironment alterations during tumorigenesis. The molecular machinery for autophagy is possibly involved in tissue architecture, neoplastic cell differentiation, and prognosis of the benign epithelial odontogenic tumor.
MeSH term(s)	Adolescent ; Adult ; Ameloblastoma/chemistry ; Ameloblastoma/pathology ; Autoantigens/analysis ; Autophagy/physiology ; Autophagy-Related Protein 7 ; Basement Membrane/chemistry ; Carcinogenesis/chemistry ; Carcinogenesis/pathology ; Cell Differentiation/physiology ; Dental Sac/chemistry ; Endothelial Cells/chemistry ; Epithelial Cells/chemistry ; Female ; Fibroblasts/chemistry ; Granular Cell Tumor/chemistry ; Granular Cell Tumor/pathology ; Humans ; Immunohistochemistry ; Male ; Microtubule-Associated Proteins/analysis ; Middle Aged ; Neoplasm Recurrence, Local/chemistry ; Neoplasm Recurrence, Local/pathology ; RNA-Binding Proteins/analysis ; Tumor Microenvironment/physiology ; Ubiquitin-Activating Enzymes/analysis
Chemical Substances	Autoantigens ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; P62 protein, human ; RNA-Binding Proteins ; ATG7 protein, human (EC 6.2.1.45) ; Autophagy-Related Protein 7 (EC 6.2.1.45) ; Ubiquitin-Activating Enzymes (EC 6.2.1.45)
Language	English
Publishing date	2014-04-25
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1021270-x
ISSN	1600-0714 ; 0904-2512
ISSN (online)	1600-0714
ISSN	0904-2512
DOI	10.1111/jop.12177
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Article ; Online: Comparison of bone regeneration between octacalcium phosphate/collagen composite and β-tricalcium phosphate in canine calvarial defect.

Tanuma, Yuji / Matsui, Keiko / Kawai, Tadashi / Matsui, Aritsune / Suzuki, Osamu / Kamakura, Shinji / Echigo, Seishi

Oral surgery, oral medicine, oral pathology and oral radiology

2013 Volume 115, Issue 1, Page(s) 9–17

Abstract: Objective: The present study evaluated the efficacy of bone regeneration between synthetic octacalcium phosphate (OCP) granules combined with porcine atelocollagen (OCP/Col) and β-tricalcium phosphate (β-TCP).: Study design: A disk of OCP/Col (20 mm ... ...

Abstract	Objective: The present study evaluated the efficacy of bone regeneration between synthetic octacalcium phosphate (OCP) granules combined with porcine atelocollagen (OCP/Col) and β-tricalcium phosphate (β-TCP). Study design: A disk of OCP/Col (20 mm diameter, 2.5 mm thick) or commercially available sintered porous β-TCP was implanted into a critical-sized calvarial defect (20 mm diameter) of adult male canines (n = 10). The newly formed bone in the defect was analyzed radiographically, crystallographically, histologically, and histomorphometrically at 6 months after implantation. Results: Histomorphometry showed that there was significantly more newly formed bone in OCP/Col-treated defects than for β-TCP (P < .05). X-Ray diffraction patterns of implanted OCP/Col were similar to those of original bone and different from those of implanted β-TCP. Conclusions: These results suggest that OCP/Col implantation in canine critical-sized defect enhanced bone regeneration more than β-TCP, which is the most commonly used synthetic bone substitutes.
MeSH term(s)	Animals ; Biocompatible Materials/pharmacology ; Bone Regeneration/drug effects ; Bone Substitutes/pharmacology ; Calcium Phosphates/pharmacology ; Collagen/pharmacology ; Dogs ; Male ; Microradiography ; Skull/diagnostic imaging ; Skull/drug effects ; X-Ray Diffraction
Chemical Substances	Biocompatible Materials ; Bone Substitutes ; Calcium Phosphates ; atelocollagen ; beta-tricalcium phosphate ; octacalcium phosphate (13767-12-9) ; Collagen (9007-34-5)
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2650843-6
ISSN	2212-4411 ; 2212-4403
ISSN (online)	2212-4411
ISSN	2212-4403
DOI	10.1016/j.oooo.2011.12.029
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Ul III Zs.121: Show issues

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Article ; Online: Rapamycin suppresses ROS-dependent apoptosis caused by selenomethionine in A549 lung carcinoma cells.

Suzuki, Maiko / Endo, Manabu / Shinohara, Fumiaki / Echigo, Seishi / Rikiishi, Hidemi

Cancer chemotherapy and pharmacology

2010 Volume 67, Issue 5, Page(s) 1129–1136

Abstract: Purpose: Although selenium compounds possess chemotherapeutic features by inducing apoptosis in cancer cells with trivial side effects on normal cells, the mechanisms underlying its anti-cancer activity are insufficiently understood at the present. In ... ...

Abstract	Purpose: Although selenium compounds possess chemotherapeutic features by inducing apoptosis in cancer cells with trivial side effects on normal cells, the mechanisms underlying its anti-cancer activity are insufficiently understood at the present. In this study, we investigated the effects of rapamycin on apoptosis induced by seleno-L-methionine (SeMet) or selenite in A549 cells. Methods: The effects of Se compounds, SeMet and selenite, on cell proliferation, apoptosis and its signaling pathway were investigated in established human adenocarcinoma cell line (A549). Cancer cells were treated with each Se during different periods. Cell apoptosis and signaling molecules were analyzed by flow cytometry (TUNEL method) or immunoblotting, respectively. Results: SeMet induces reactive oxygen species generation associated with the induction of apoptosis, because pretreatment of cells with N-acetyl-L-cysteine completely blocked SeMet-induced apoptosis. We also found that rapamycin completely suppressed the apoptosis of cells treated by SeMet, but not selenite. SeMet-induced apoptosis is significantly downregulated in combination with PI3 K family inhibitors (LY294002, wortmannin, PI-103, and 3-methyladenine). In addition, ROS generation was included in downstream signaling events associated with the phosphorylation of mTOR, because pretreatment of cells with rapamycin inhibited ROS generation. Conclusion: These results suggest that SeMet-induced apoptosis is affected by the Akt/mTOR/ROS pathway in A549 cells. Akt serves an anti-survival function in the system of SeMet-treated lung cancer cells, but autophagic signaling remained unsolved.
MeSH term(s)	Adenocarcinoma ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Autophagy/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Humans ; Lung Neoplasms ; Microtubule-Associated Proteins/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Phosphorylation ; Proto-Oncogene Proteins c-akt/physiology ; Reactive Oxygen Species/metabolism ; Selenomethionine/pharmacology ; Signal Transduction ; Sirolimus/pharmacology ; Sodium Selenite/pharmacology ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Antineoplastic Agents ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Phosphoinositide-3 Kinase Inhibitors ; Reactive Oxygen Species ; Selenomethionine (964MRK2PEL) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Sodium Selenite (HIW548RQ3W) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2010-08-03
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6820-2
ISSN	1432-0843 ; 0344-5704 ; 0943-9404
ISSN (online)	1432-0843
ISSN	0344-5704 ; 0943-9404
DOI	10.1007/s00280-010-1417-7
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Zs.A 1420: Show issues

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Article ; Online: Effects of mevastatin on grafted bone in MRL/MpJ mice.

Sugazaki, Masaki / Hirotani, Hiroaki / Echigo, Seishi / Takeyama, Sadaaki / Shinoda, Hisashi

Connective tissue research

2010 Volume 51, Issue 2, Page(s) 105–112

Abstract: Statins, lipid-lowering drugs, have been reported to influence bone metabolism. However, the available information about their effects on bone formation and resorption in vivo is still limited. The present study was undertaken to determine whether the ... ...

Abstract	Statins, lipid-lowering drugs, have been reported to influence bone metabolism. However, the available information about their effects on bone formation and resorption in vivo is still limited. The present study was undertaken to determine whether the topical administration of mevastatin could increase the bone mass of isografted bone. The tibiae were bilaterally dissected from a donor MRL/MpJ mouse and transplanted subcutaneously in the dorsal region of a recipient mouse. One grafted tibia was topically infused for either 1, 2, 3, or 4 weeks with mevastatin, using an osmotic minipump at a dose of 2.5 pmol/hr. The other tibia was infused with 0.9% NaCl (control). Our three results were: (1) Topical mevastatin stimulated bone formation and numerous cuboidal osteoblasts appeared on the surface of newly formed bone. Bone mineral density and bone area in mevastatin-treated bone were significantly increased. (2) Topical mevastatin increased the number of osteoclasts. (3) The expression of bone morphogenetic protein-2 (BMP-2) mRNA and receptor activator of NF-kB ligand (RANKL) mRNA were upregulated in mevastatin-treated bone. These results suggest that the topical infusion of mevastatin increases bone mass of isografted bone by increasing bone turnover and, at least in part, by promoting the expression of BMP-2 and RANKL mRNA.
MeSH term(s)	Administration, Topical ; Animals ; Anticholesteremic Agents/pharmacology ; Bone Density/drug effects ; Bone Morphogenetic Protein 2/genetics ; Bone Morphogenetic Protein 2/metabolism ; Bone Transplantation ; Cell Count ; Disease Models, Animal ; Lovastatin/analogs & derivatives ; Lovastatin/pharmacology ; Male ; Mice ; Mice, Inbred MRL lpr ; Osteoclasts/drug effects ; Osteoclasts/pathology ; Osteogenesis ; RANK Ligand/genetics ; RANK Ligand/metabolism ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Tibia/drug effects ; Tibia/metabolism ; Tibia/transplantation ; Up-Regulation/drug effects
Chemical Substances	Anticholesteremic Agents ; Bmp2 protein, mouse ; Bone Morphogenetic Protein 2 ; RANK Ligand ; RNA, Messenger ; Tnfsf11 protein, mouse ; mevastatin (1UQM1K0W9X) ; Lovastatin (9LHU78OQFD)
Language	English
Publishing date	2010-04
Publishing country	England
Document type	Journal Article
ZDB-ID	185551-7
ISSN	1607-8438 ; 0091-1690 ; 0300-8207
ISSN (online)	1607-8438
ISSN	0091-1690 ; 0300-8207
DOI	10.3109/03008200903105098
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Zs.A 1093: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Differential apoptotic response of human cancer cells to organoselenium compounds.

Suzuki, Maiko / Endo, Manabu / Shinohara, Fumiaki / Echigo, Seishi / Rikiishi, Hidemi

Cancer chemotherapy and pharmacology

2010 Volume 66, Issue 3, Page(s) 475–484

Abstract: Purpose: Selenium (Se) compounds are well known to inhibit cell proliferation and induce cell death in human cancer cells. Respective chemical forms of Se are intracellularly metabolized via complicated pathways, which target distinct molecules and ... ...

Abstract	Purpose: Selenium (Se) compounds are well known to inhibit cell proliferation and induce cell death in human cancer cells. Respective chemical forms of Se are intracellularly metabolized via complicated pathways, which target distinct molecules and exhibit varying degrees of anti-carcinogenicity in different cancer types; however, the precise mechanisms by which Se activates apoptosis remain poorly understood. Methods: The effects of Se compounds, Se-methylselenocysteine (MSC), selenomethionine (SeMet), and selenite on cell proliferation, apoptosis and its pathway in established human carcinoma cell lines (HSC-3, -4, A549, and MCF-7) were investigated. Cancer cells were treated with each Se compound during different periods. Cell apoptosis, caspase activity and ER stress markers were analyzed by flow cytometric or immunoblotting analysis, respectively. Results: We examined four cell lines for their sensitivity to MSC and SeMet in comparison with selenite. SeMet increased apoptotic cells in p53-positive A549 cells, whereas MSC increased apoptotic cells in p53-mutated HSC-3 cells. High activities of caspase-3, -8 and -9 were observed during apoptosis, and a pan-caspase inhibitor, z-VAD-fmk, rescued the cell viability of HSC-3 cells exposed to MSC. In addition, the occurrence of endoplasmic reticulum (ER) stress was suggested by the observation that levels of phosphorylated eIF2alpha and caspase-12 activity are increased in Se-treated cells. Selenite and MSC were accompanied with the concurrent reduction of phosphorylated Akt levels, and the inhibitory effects of these Se compounds on vascular endothelial growth factor expression were observed with identical patterns. Conclusion: The present findings demonstrate that Se-induced apoptosis in carcinoma cells is basically a caspase-dependent process involving complicated mechanisms. Activation of both the intrinsic apoptotic pathway and ER stress pathway plays a major and concurrent role, while p53 activation seems to have only a functional role in SeMet.
MeSH term(s)	Anticarcinogenic Agents/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Caspase 3/drug effects ; Caspase 8/drug effects ; Caspase 8/metabolism ; Caspase 9/drug effects ; Caspase 9/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cysteine/analogs & derivatives ; Cysteine/pharmacology ; Flow Cytometry ; Humans ; Neoplasms/drug therapy ; Neoplasms/pathology ; Organoselenium Compounds/pharmacology ; Selenocysteine/analogs & derivatives ; Selenomethionine/pharmacology ; Sodium Selenite/pharmacology ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Anticarcinogenic Agents ; Organoselenium Compounds ; Tumor Suppressor Protein p53 ; Selenocysteine (0CH9049VIS) ; Selenomethionine (964MRK2PEL) ; Caspase 3 (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-) ; Sodium Selenite (HIW548RQ3W) ; Cysteine (K848JZ4886) ; selenomethylselenocysteine (TWK220499Z)
Language	English
Publishing date	2010-08
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6820-2
ISSN	1432-0843 ; 0344-5704 ; 0943-9404
ISSN (online)	1432-0843
ISSN	0344-5704 ; 0943-9404
DOI	10.1007/s00280-009-1183-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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