STAT-1-independent upregulation of FADD and procaspase-3 and -8 in cancer cells treated with cytotoxic drugs

被引：53

作者：

Micheau, O ^{[1
]}

Hammann, A ^{[1
]}

Solary, E ^{[1
]}

Dimanche-Boitrel, MT ^{[1
]}

机构：

[1] Fac Med & Pharm, Dept Biol & Therapy Canc JE515, NSERM U517, F-21033 Dijon, France

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1999年 / 256卷 / 03期

关键词：

anticancer drugs; FAS; FADD; caspases; apoptosis;

D O I：

10.1006/bbrc.1999.0391

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

We have previously shown that treatment by anticancer drugs sensitized tumor cells to Fas (APO-1/CD95)-mediated cell death. The present study demonstrates that the cytotoxic drugs cisplatin, doxorubicin and mitomycin C induce the accumulation of the Fas receptor, the FADD adaptor molecule, the procaspases-8, -3 and -2L and the proapoptotic molecule Bar in several human colon cancer cells. This upregulation is also observed in U3A myeloblastoma cells that do not express STAT-1, a transcription factor involved in the constitutive expression of procaspases. We conclude that anticancer drugs sensitize tumor cells to Fas-mediated cell death by a STAT-1-independent upregulation of molecules involved in this apoptotic pathway, (C) 1999 Academic Press.

引用

页码：603 / 607

页数：5

共 30 条

[11] Caspases are activated in a branched protease cascade and control distinct downstream processes in Fas-induced apoptosis [J].

Hirata, H ;

Takahashi, A ;

Kobayashi, S ;

Yonehara, S ;

Sawai, H ;

Okazaki, T ;

Yamamoto, K ;

Sasada, M .

JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (04) :587-600

[12] THE POLYPEPTIDE ENCODED BY THE CDNA FOR HUMAN CELL-SURFACE ANTIGEN FAS CAN MEDIATE APOPTOSIS [J].

ITOH, N ;

YONEHARA, S ;

ISHII, A ;

YONEHARA, M ;

MIZUSHIMA, S ;

SAMESHIMA, M ;

HASE, A ;

SETO, Y ;

NAGATA, S .

CELL, 1991, 66 (02) :233-243

[13] Prevention of constitutive TNF receptor 1 signaling by silencer of death domains [J].

Jiang, YP ;

Woronicz, JD ;

Liu, W ;

Goeddel, DV .

SCIENCE, 1999, 283 (5401) :543-546

[14] MCL1, A GENE EXPRESSED IN PROGRAMMED MYELOID CELL-DIFFERENTIATION, HAS SEQUENCE SIMILARITY TO BCL2 [J].

KOZOPAS, KM ;

YANG, T ;

BUCHAN, HL ;

ZHOU, P ;

CRAIG, RW .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (08) :3516-3520

[15] Defective TNF-alpha-induced apoptosis in STAT1-null cells due to low constitutive levels of caspases [J].

Kumar, A ;

Commane, M ;

Flickinger, TW ;

Horvath, CM ;

Stark, GR .

SCIENCE, 1997, 278 (5343) :1630-1632

[16] FLICE is activated by association with the CD95 death-inducing signaling complex (DISC) [J].

Medema, JP ;

Scaffidi, C ;

Kischkel, FC ;

Shevchenko, A ;

Mann, M ;

Krammer, PH ;

Peter, ME .

EMBO JOURNAL, 1997, 16 (10) :2794-2804

[17] Sensitization of cancer cells treated with cytotoxic drugs to Fas-mediated cytotoxicity [J].

Micheau, O ;

Solary, E ;

Hammann, A ;

Martin, F ;

DimancheBoitrel, MT .

JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1997, 89 (11) :783-789

[18]

MICHEAU O, 1999, IN PRESS J BIOL CHEM

[19] Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53 [J].

Muller, M ;

Strand, S ;

Hug, H ;

Heinemann, EM ;

Walczak, H ;

Hofmann, WJ ;

Stremmel, W ;

Krammer, PH ;

Galle, PR .

JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (03) :403-413

[20] FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex [J].

Muzio, M ;

Chinnaiyan, AM ;

Kischkel, FC ;

ORourke, K ;

Shevchenko, A ;

Ni, J ;

Scaffidi, C ;

Bretz, JD ;

Zhang, M ;

Gentz, R ;

Mann, M ;

Krammer, PH ;

Peter, ME ;

Dixit, VM .

CELL, 1996, 85 (06) :817-827

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