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Article ; Online: Novel Insights into the Interplay between Apoptosis and Autophagy.

Rikiishi, Hidemi

2012 Volume 2012, Page(s) 317645

Abstract: For several decades, apoptosis has taken center stage as the principal mechanism of programmed cell death (type I cell death) in mammalian tissues. Autophagic cell death (type II) is characterized by the massive accumulation of autophagic vacuoles in the ...

Abstract	For several decades, apoptosis has taken center stage as the principal mechanism of programmed cell death (type I cell death) in mammalian tissues. Autophagic cell death (type II) is characterized by the massive accumulation of autophagic vacuoles in the cytoplasm of cells. The autophagic process is activated as an adaptive response to a variety of extracellular and intracellular stresses, including nutrient deprivation, hormonal or therapeutic treatment, pathogenic infection, aggregated and misfolded proteins, and damaged organelles. Increasing evidence indicates that autophagy is associated with a number of pathological processes, including cancer. The regulation of autophagy in cancer cells is complex since it can enhance cancer cell survival in response to certain stresses, while it can also act to suppress the initiation of cancer growth. This paper focused on recent advances regarding autophagy in cancer and the techniques currently available to manipulate autophagy.
Language	English
Publishing date	2012-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2536742-0
ISSN	1687-8884 ; 1687-8884
ISSN (online)	1687-8884
ISSN	1687-8884
DOI	10.1155/2012/317645
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Autophagic action of new targeting agents in head and neck oncology.

Rikiishi, Hidemi

Cancer biology & therapy

2012 Volume 13, Issue 11, Page(s) 978–991

Abstract: The survival rates of patients with squamous cell carcinoma of the head and neck (HNSCC) have not improved significantly despite multi-modality therapy, including surgery, radiation therapy, and chemotherapy. Recently, molecular targeted agents have ... ...

Abstract	The survival rates of patients with squamous cell carcinoma of the head and neck (HNSCC) have not improved significantly despite multi-modality therapy, including surgery, radiation therapy, and chemotherapy. Recently, molecular targeted agents have shown significant improvement in clinical outcomes; for example, in chronic myelogeneous leukemia with imatinib, breast cancer with trastuzumab, colon cancer with bevacizumab and cetuximab, and renal cell cancer with sorafenib and sunitinib. In HNSCC, the epidermal growth factor receptor antibody cetuximab has shown promising results in combination with radiation. Targeted agents including cetuximab induce stresses to activate prosurvival autophagy. Combining autophagy inhibitors with agents that induce autophagy as a prosurvival response may therefore increase their therapeutic efficacy. Whether autophagy contributes to the prosurvival response or to the antitumor effect of chemotherapeutic drugs is largely unknown. This review will discuss the possible role of autophagy as a novel target for anticancer therapy agents in HNSCC.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Autophagy/drug effects ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/enzymology ; Carcinoma, Squamous Cell/pathology ; Head and Neck Neoplasms/drug therapy ; Head and Neck Neoplasms/enzymology ; Head and Neck Neoplasms/pathology ; Humans ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Squamous Cell Carcinoma of Head and Neck
Chemical Substances	Antineoplastic Agents ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2012-07-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2146305-0
ISSN	1555-8576 ; 1538-4047
ISSN (online)	1555-8576
ISSN	1538-4047
DOI	10.4161/cbt.21079
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Zs.A 5887: Show issues

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Article ; Online: Novel Insights into the Interplay between Apoptosis and Autophagy

Hidemi Rikiishi

International Journal of Cell Biology, Vol

2012 Volume 2012

Keywords	Cytology ; QH573-671 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Cytology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Hindawi Publishing Corporation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Autophagic and apoptotic effects of HDAC inhibitors on cancer cells.

Rikiishi, Hidemi

Journal of biomedicine & biotechnology

2011 Volume 2011, Page(s) 830260

Abstract: Because epigenetic alterations are believed to be involved in the repression of tumor suppressor genes and the promotion of tumorigenesis in cancers, novel compounds endowed with histone deacetylase (HDAC) inhibitory activity are an attractive ... ...

Abstract	Because epigenetic alterations are believed to be involved in the repression of tumor suppressor genes and the promotion of tumorigenesis in cancers, novel compounds endowed with histone deacetylase (HDAC) inhibitory activity are an attractive therapeutic approach. Indeed, the potential of HDAC inhibitors for cancer therapy has been explored in preclinical models, and some agents approved for hematologic malignancies have reached the clinical setting. HDAC inhibitors are able to mediate the induction of both apoptosis and autophagy, which are related to anticancer activity in a variety of cancer cell lines. Given the inherent resistance to apoptosis that characterizes cancer, the targeting of alternative pathways is an attractive strategy to improve anti-tumor therapy. The activation of autophagy represents novel cancer treatment targets. This paper aims to critically discuss how the anticancer potential of HDAC inhibitors may elicit a response to human cancers through different cell pathways leading to cell death.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Autophagy/drug effects ; Histone Deacetylase Inhibitors/administration & dosage ; Histone Deacetylases/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism
Chemical Substances	Histone Deacetylase Inhibitors ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2011-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052552-7
ISSN	1110-7251 ; 1110-7243
ISSN (online)	1110-7251
ISSN	1110-7243
DOI	10.1155/2011/830260
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Zs.A 5540: Show issues

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Article: Possible role of autophagy in the treatment of pancreatic cancer with histone deacetylase inhibitors.

Rikiishi, Hidemi

Cancers

2010 Volume 2, Issue 4, Page(s) 2026–2043

Abstract: Pancreatic cancer is a lethal disease and notoriously difficult to treat. Only a small proportion is curative by surgical resection, whilst standard chemotherapy for patients with advanced disease has only a modest effect with substantial toxicity. ... ...

Abstract	Pancreatic cancer is a lethal disease and notoriously difficult to treat. Only a small proportion is curative by surgical resection, whilst standard chemotherapy for patients with advanced disease has only a modest effect with substantial toxicity. Clearly there is a need for the continual development of novel therapeutic agents to improve the current situation. Currently, there is a bulk of data indicating the important function of autophagy in cancer. While genetic evidence indicates that autophagy functions as a tumor suppressor, it is also apparent that autophagy can promote the survival of established tumors under stress conditions and in response to chemotherapy. This review provides a spectrum of potential pharmacological agents and autophagic approaches to enhance cell killing in pancreatic cancer.
Language	English
Publishing date	2010-11-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers2042026
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Article ; Online: Autophagic and Apoptotic Effects of HDAC Inhibitors on Cancer Cells

Hidemi Rikiishi

Journal of Biomedicine and Biotechnology, Vol

2011 Volume 2011

Abstract	Because epigenetic alterations are believed to be involved in the repression of tumor suppressor genes and the promotion of tumorigenesis in cancers, novel compounds endowed with histone deacetylase (HDAC) inhibitory activity are an attractive therapeutic approach. Indeed, the potential of HDAC inhibitors for cancer therapy has been explored in preclinical models, and some agents approved for hematologic malignancies have reached the clinical setting. HDAC inhibitors are able to mediate the induction of both apoptosis and autophagy, which are related to anticancer activity in a variety of cancer cell lines. Given the inherent resistance to apoptosis that characterizes cancer, the targeting of alternative pathways is an attractive strategy to improve anti-tumor therapy. The activation of autophagy represents novel cancer treatment targets. This paper aims to critically discuss how the anticancer potential of HDAC inhibitors may elicit a response to human cancers through different cell pathways leading to cell death.
Keywords	Biotechnology ; TP248.13-248.65 ; Medicine ; R
Subject code	610
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Possible Role of Autophagy in the Treatment of Pancreatic Cancer with Histone Deacetylase Inhibitors

Hidemi Rikiishi

Cancers, Vol 2, Iss 4, Pp 2026-

2010 Volume 2043

Abstract	Pancreatic cancer is a lethal disease and notoriously difficult to treat. Only a small proportion is curative by surgical resection, whilst standard chemotherapy for patients with advanced disease has only a modest effect with substantial toxicity. Clearly there is a need for the continual development of novel therapeutic agents to improve the current situation. Currently, there is a bulk of data indicating the important function of autophagy in cancer. While genetic evidence indicates that autophagy functions as a tumor suppressor, it is also apparent that autophagy can promote the survival of established tumors under stress conditions and in response to chemotherapy. This review provides a spectrum of potential pharmacological agents and autophagic approaches to enhance cell killing in pancreatic cancer.
Keywords	pancreatic cancer ; autophagy ; apoptosis ; epigenetics ; histone deacetylase ; ER stress ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2010-11-01T00:00:00Z
Publisher	Molecular Diversity Preservation International
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Apoptotic cellular events for selenium compounds involved in cancer prevention.

Rikiishi, Hidemi

Journal of bioenergetics and biomembranes

2007 Volume 39, Issue 1, Page(s) 91–98

Abstract: Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer ... ...

Abstract	Converging data from epidemiological, ecological, and clinical studies have shown that selenium (Se) can decrease the risk for some types of human cancers. Induction of apoptosis is considered an important cellular event that can account for the cancer preventive effects of Se. Prior to occurrence of apoptosis, Se compounds alter the expression and/or activities of signaling molecules, mitochondria-associated factors, transcriptional factors, tumor suppressor genes, and cellular reduced glutathione. Mechanistic studies have demonstrated that the methylselenol metabolite pool has many desirable attributes of chemoprevention, whereas the hydrogen selenide pool with excess of selenoprotein synthesis can lead to DNA single-strand breaks. To elucidate the effects of Se on cytotoxic events, it should be remembered that the chemical forms and the dose of Se, and the experimental system used, are determinants of its biological activities. This mini-review focuses on elucidation of the molecular mechanisms of cancer prevention by Se with the apoptotic approach.
MeSH term(s)	Anticarcinogenic Agents/pharmacology ; Anticarcinogenic Agents/therapeutic use ; Apoptosis/drug effects ; Apoptosis/physiology ; DNA Breaks, Single-Stranded ; Humans ; Methanol/analogs & derivatives ; Neoplasms/prevention & control ; Organometallic Compounds/pharmacology ; Organometallic Compounds/therapeutic use ; Organoselenium Compounds ; Selenium/pharmacology ; Selenium/therapeutic use ; Selenium Compounds/pharmacology ; Selenium Compounds/therapeutic use ; Selenoproteins/biosynthesis
Chemical Substances	Anticarcinogenic Agents ; Organometallic Compounds ; Organoselenium Compounds ; Selenium Compounds ; Selenoproteins ; methaneselenol (60343-91-1) ; Selenium (H6241UJ22B) ; hydrogen selenide (V91P54KPAM) ; Methanol (Y4S76JWI15)
Language	English
Publishing date	2007-02-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	198499-8
ISSN	1573-6881 ; 0145-479X ; 0449-5705
ISSN (online)	1573-6881
ISSN	0145-479X ; 0449-5705
DOI	10.1007/s10863-006-9065-7
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Zs.A 1005: Show issues

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Article ; Online: Agarol, an ergosterol derivative from Agaricus blazei, induces caspase-independent apoptosis in human cancer cells.

Shimizu, Takamitsu / Kawai, Junya / Ouchi, Kenji / Kikuchi, Haruhisa / Osima, Yoshiteru / Hidemi, Rikiishi

International journal of oncology

2016 Volume 48, Issue 4, Page(s) 1670–1678

Abstract: Agaricus blazei (A. blazei) is a mushroom with many biological effects and active ingredients. We purified a tumoricidal substance from A. blazei, an ergosterol derivative, and named it 'Agarol'. Cytotoxic effects of Agarol were determined by the MTT ... ...

Abstract	Agaricus blazei (A. blazei) is a mushroom with many biological effects and active ingredients. We purified a tumoricidal substance from A. blazei, an ergosterol derivative, and named it 'Agarol'. Cytotoxic effects of Agarol were determined by the MTT assay using A549, MKN45, HSC-3, and HSC-4 human carcinoma cell lines treated with Agarol. Apoptosis was detected by flow cytometry analysis. Reactive oxygen species (ROS) levels and mitochondria membrane potential (∆ψm) were also determined by flow cytometry. Western blot analysis was used to quantify the expression of apoptosis-related proteins. Agarol predominantly induced apoptosis in two p53-wild cell lines (A549 and MKN45) compared to the other p53-mutant cell lines (HSC-3 and HSC-4). Further mechanistic studies revealed that induction of apoptosis is associated with increased generation of ROS, reduced ∆ψm, release of apoptosis-inducing factor (AIF) from the mitochondria to the cytosol, upregulation of Bax, and downregulation of Bcl-2. Caspase-3 activities did not increase, and z-VAD-fmk, a caspase inhibitor, did not inhibit the Agarol-induced apoptosis. These findings indicate that Agarol induces caspase-independent apoptosis in human carcinoma cells through a mitochondrial pathway. The in vivo anticancer activity of Agarol was confirmed in a xenograft murine model. This study suggests a molecular mechanism by which Agarol induces apoptosis in human carcinoma cells and indicates the potential use of Agarol as an anticancer agent.
MeSH term(s)	Agaricus/chemistry ; Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Apoptosis ; Caspases/metabolism ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Ergosterol/administration & dosage ; Ergosterol/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Membrane Potential, Mitochondrial/drug effects ; Mice ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Reactive Oxygen Species ; Caspases (EC 3.4.22.-) ; Ergosterol (Z30RAY509F)
Language	English
Publishing date	2016-04
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2016.3391
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Zs.A 3690: Show issues

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Article: Zebularine-induced reduction in VEGF secretion by HIF-1α degradation in oral squamous cell carcinoma.

Suzuki, Maiko / Shinohara, Fumiaki / Rikiishi, Hidemi

Molecular medicine reports

2008 Volume 1, Issue 4, Page(s) 465–471

Abstract: Vascular endothelial growth factor (VEGF) is a potent inducer of angiogenesis in oral squamous cell carcinoma (OSCC). In this study, we used the novel DNA methyltransferase inhibitor zebularine (Zeb) to investigate epigenetic influences on the secretion ... ...

Abstract	Vascular endothelial growth factor (VEGF) is a potent inducer of angiogenesis in oral squamous cell carcinoma (OSCC). In this study, we used the novel DNA methyltransferase inhibitor zebularine (Zeb) to investigate epigenetic influences on the secretion of VEGF-A in the OSCC cell line HSC-3. Under normoxic conditions, we found that Zeb inhibited secretion in a dose-dependent manner by reducing the activity of hypoxia-inducible factor-1α (HIF-1α). Treatment of the cells with the proteasome inhibitor MG132 protected the HIF-1α protein from Zeb-mediated epigenetic regulation. In addition, our study revealed that neither the PI3K/Akt nor the p53 signaling pathway is required for Zeb-induced HIF-1α degradation. In short, Zeb influenced the stability of the HIF-1α protein and the activity of its targets, such as VEGF, in HSC-3 cells in normoxic conditions. This study has laid the foundation for a novel anti-cancer approach, which may find applications in molecular staging.
Language	English
Publishing date	2008-07
Publishing country	Greece
Document type	Journal Article
ISSN	1791-2997
ISSN	1791-2997
Database	MEDical Literature Analysis and Retrieval System OnLINE

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