학제간연구 | Interdisciplinary Studies in Gambling | 跨学科研究
- date : 2015-05-20 01:10|hit : 1431
-
- Article] Differential involvement of mitochondria during ursolic acid-induced apoptotic process in HaCaT and M4Beu cells
-
DocNo of ILP: 4003
Doc. Type: Article
Title: Differential involvement of mitochondria during ursolic acid-induced apoptotic process in HaCaT and M4Beu cells
Authors: Duval, RE; Harmand, PO; Jayat-Vignoles, C; Cook-Moreau, J; Pinon, A; Delage, C; Simon, A
Full Name of Authors: Duval, Raphael Emmanuel; Harmand, Pierre-Olivier; Jayat-Vignoles, Chantal; Cook-Moreau, Jeanne; Pinon, Aline; Delage, Christiane; Simon, Alain
Keywords by Author: ursolic acid; HaCaT; M4Beu; apoptosis; mitochondria
Keywords Plus: BCL-2 PROTEIN FAMILY; OLEANOLIC ACID; CASPASE-3 ACTIVATION; DEPENDENT APOPTOSIS; DEATH; INHIBITION; PATHWAY; ARREST; JC-1
Abstract: Ursolic acid (UA) is a pentacyclic triterpenoid compound which exists widely in nature and is known to have a pleitropic biological activity profile. For the last few decades, extensive work has been carried out to establish its biological activities and pharmacological actions. It is described as a promising chemopreventive agent with an antiproliferative effect on cancer cells that stems from its ability to induce apoptosis. We investigated and compared the role played by mitochondria during the apoptotic process induced by UA in human HaCaT-derived keratinotic cells and M4Beu human melanoma cells. In both cell lines, UA induced significant caspase-3 activation, the downstream central effector of apoptosis. Subsequent JC-1/TOTO-3 double staining clearly demonstrated that UA induces strong mitochondrial-transmembrane potential collapse in M4Beu cells, while mitochondria from HaCaT-treated cells remain largely unstimulated. This was confirmed by Western blot analysis, which revealed a Bax/Bcl-2-balance change in favor of Bax, the proapoptotic member, in UA-treated M4Beu cells. It can be concluded that UA induces apoptosis in M4Beu through the mitochondrial pathway, while other mechanisms are activated in the case of HaCaT cells.
Cate of OECD: Clinical medicine
Year of Publication: 2008
Business Area: other
Detail Business: medicine & science
Country: USA
Study Area:
Name of Journal: ONCOLOGY REPORTS
Language: English
Country of Authors: [Duval, Raphael Emmanuel; Harmand, Pierre-Olivier; Pinon, Aline; Delage, Christiane; Simon, Alain] Fac Pharm, Chim Phys Lab, EA 4021, F-87025 Limoges, France; [Jayat-Vignoles, Chantal] CNRS, UMR 6101, Fac Med, F-87025 Limoges, France; [Cook-Moreau, Jeanne] Fac Med, Lab Biochim Med, F-87025 Limoges, France
Press Adress: Simon, A (reprint author), Fac Pharm, Chim Phys Lab, EA 4021, 2 Rue Docteur Marcland, F-87025 Limoges, France.
Email Address: simon@unilim.fr
Citaion:
Funding:
Lists of Citation: Achiwa Y, 2005, ONCOL REP, V13, P51; Achiwa Y, 2005, ONCOL REP, V14, P507; Alnemri ES, 1996, CELL, V87, P171, DOI 10.1016/S0092-8674(00)81334-3; Antonsson B, 2000, EXP CELL RES, V256, P50, DOI 10.1006/excr.2000.4839; Baek JH, 1997, INT J CANCER, V73, P725, DOI 10.1002/(SICI)1097-0215(19971127)73:5<725::AID-IJC19>3.0.CO;2-4; Borner C, 2003, MOL IMMUNOL, V39, P615, DOI 10.1016/S0161-5890(02)00252-3; COSSARIZZA A, 1993, BIOCHEM BIOPH RES CO, V197, P40, DOI 10.1006/bbrc.1993.2438; DARZYNKIEWICZ Z, 1982, CANCER RES, V42, P799; Earnshaw WC, 1999, ANNU REV BIOCHEM, V68, P383, DOI 10.1146/annurev.biochem.68.1.383; Harmand PO, 2005, INT J CANCER, V114, P1, DOI 10.1002/ijc.20588; Harmand PO, 2003, INT J ONCOL, V23, P105; Hollosy F, 2001, ANTICANCER RES, V21, P3485; Hsu YL, 2004, LIFE SCI, V75, P2303, DOI 10.1016/j.lfs.2004.04.027; HUANG MT, 1994, CANCER RES, V54, P701; Kroemer G, 2000, NAT MED, V6, P513, DOI 10.1038/74994; Kroemer G, 2001, B ACAD NAT MED PARIS, V185, P1135; Lauthier F, 2000, ANTI-CANCER DRUG, V11, P737; Lee YS, 2003, EUR J PHARMACOL, V476, P173, DOI 10.1016/S0014-2999(03)02177-0; Liu H, 2005, J ETHNOPHARMACOL, V100, P92, DOI 10.1016/j.jep.2005.05.024; Liu J, 1995, J ETHNOPHARMACOL, V49, P57, DOI 10.1016/0378-8741(95)90032-2; Loeffler M, 2000, EXP CELL RES, V256, P19, DOI 10.1006/excr.2000.4833; Novotny L, 2001, NEOPLASMA, V48, P241; Ovesna Z, 2004, NEOPLASMA, V51, P327; Reed JC, 1998, BBA-BIOENERGETICS, V1366, P127, DOI 10.1016/S0005-2728(98)00108-X; Rona C, 2004, J Cosmet Dermatol, V3, P26, DOI 10.1111/j.1473-2130.2004.00054.x; Roy S, 2000, J EXP MED, V192, P21; Satomi Y, 2005, ANTICANCER RES, V25, P4043; SHAPIRO HM, 1994, METHOD CELL BIOL, V41, P121; Stennicke HR, 1998, J BIOL CHEM, V273, P27084, DOI 10.1074/jbc.273.42.27084; TOKUDA H, 1986, CANCER LETT, V33, P279, DOI 10.1016/0304-3835(86)90067-4; Yarosh DB, 2000, HORM RES, V54, P318, DOI 10.1159/000053280; Zuliani T, 2003, CYTOM PART A, V54A, P100, DOI 10.1002/cyto.a.10059
Number of Citaion: 32
Publication: PROFESSOR D A SPANDIDOS
City of Publication: ATHENS
Address of Publication: 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE
ISSN: 1021-335X
29-Character Source Abbreviation: ONCOL REP
ISO Source Abbreviation: Oncol. Rep.
Volume: 19
Version: 1
Start of File: 145
End of File: 149
DOI:
Number of Pages: 5
Web of Science Category: Oncology
Subject Category: Oncology
Document Delivery Number: 246VT
Unique Article Identifier: WOS:000252036500020
- reply : 0
-
- list
-
- prev
- next