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Research article

Abundant expression of Dec1/stra13/sharp2 in colon carcinoma: its antagonizing role in serum deprivation-induced apoptosis and selective inhibition of procaspase activation

Yuxin LI, He ZHANG, Mingxing XIE, Maowen HU, Shujun GE, Dongfang YANG, Yinsheng WAN, Bingfang YAN
Biochemical Journal Oct 15, 2002, 367 (2) 413-422; DOI: 10.1042/bj20020514
Yuxin LI
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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He ZHANG
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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Mingxing XIE
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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Maowen HU
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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Shujun GE
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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Dongfang YANG
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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Yinsheng WAN
Department of Biology, Providence College, Providence, RI 02908, U.S.A.
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Bingfang YAN
Department of Biomedical Sciences, University of Rhode Island, Kingston, RI 02881, U.S.A.,
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Abstract

The basic helix—loop—helix (bHLH) proteins are intimately associated with developmental events such as cell differentiation and lineage commitment. The HLH domain in the bHLH motif is responsible for dimerization, whereas the basic region mediates DNA binding. Based on sequence alignment and domain analysis, differentially expressed in chondrocytes/stimulated with retinoic acid/split and hairy-related proteins (DEC/STRA/SHARPs) represent a new class of bHLH proteins. The present study describes the functional characterization of DEC1. Subtractive experiments and blotting analyses demonstrated that DEC1 was highly expressed in colon carcinomas, but not in the adjacent normal tissues. Several cell cycle blockers markedly induced DEC1 expression. Stable transfectants with a tetracycline-inducible construct demonstrated that DEC1 caused proliferation inhibition, antagonized serum deprivation-induced apoptosis and selectively inhibited the activation of procaspases. These activities were highly correlated with the abundance of tetracycline-induced DEC1. Stable transfectants expressing a mutant DEC1 (lacking the DNA-binding domain) exhibited neither proliferation inhibition nor apoptotic antagonism, which suggests that DNA binding is required for these actions. Enzymic assays and immunoblotting analyses demonstrated that induction of DEC1 by tetracycline significantly decreased the activation of procaspases 3, 7 and 9 but not procaspase 8. The selective suppression on the activation of procaspases 3, 7 and 9 over procaspase 8 suggests that DEC1-mediated anti-apoptosis is achieved by blocking apoptotic pathways initiated via the mitochondria. The results functionally distinguish DEC1 from other bHLH proteins and directly link this factor to oncogenesis.

  • basic helix–loop–helix
  • proliferation inhibition
  • transcription factor

Footnotes

  • Abbreviations used: bHLH, basic helix—loop—helix; DEC, differentially expressed in chondrocytes; DMEM, Dulbecco's modified Eagle's medium; DTT, dithiothreitol; E(spl), enhancer of split; HIF-1, hypoxia-inducible factor 1; poly(A)+, polyadenylated; SHARP, split and hairy-related protein; STRA, stimulated with retinoic acid.

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October 2002

Volume: 367 Issue: 2

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Abundant expression of Dec1/stra13/sharp2 in colon carcinoma: its antagonizing role in serum deprivation-induced apoptosis and selective inhibition of procaspase activation
Yuxin LI, He ZHANG, Mingxing XIE, Maowen HU, Shujun GE, Dongfang YANG, Yinsheng WAN, Bingfang YAN
Biochemical Journal Oct 2002, 367 (2) 413-422; DOI: 10.1042/bj20020514
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Abundant expression of Dec1/stra13/sharp2 in colon carcinoma: its antagonizing role in serum deprivation-induced apoptosis and selective inhibition of procaspase activation
Yuxin LI, He ZHANG, Mingxing XIE, Maowen HU, Shujun GE, Dongfang YANG, Yinsheng WAN, Bingfang YAN
Biochemical Journal Oct 2002, 367 (2) 413-422; DOI: 10.1042/bj20020514

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Keywords

basic helix–loop–helix
proliferation inhibition
transcription factor

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