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Gene Review

DDIT3  -  DNA-damage-inducible transcript 3

Homo sapiens

Synonyms: C/EBP zeta, C/EBP-homologous protein, C/EBP-homologous protein 10, CCAAT/enhancer-binding protein homologous protein, CEBPZ, ...
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Disease relevance of DDIT3


High impact information on DDIT3


Chemical compound and disease context of DDIT3


Biological context of DDIT3


Anatomical context of DDIT3


Associations of DDIT3 with chemical compounds


Physical interactions of DDIT3

  • The TLS-CHOP oncoprotein, found in the majority of human myxoid liposarcomas, consists of a fusion between the transcription factor CHOP/GADD153 and the N terminus of an RNA-binding protein TLS/FUS [21].

Regulatory relationships of DDIT3

  • The growth arrest- and DNA damage-inducible gene 153 (GADD153) mRNA expression was prominently upregulated by CRP [22].
  • Taken together, these results strongly suggest that ATF3 represses the expression of gadd153/Chop10 [23].
  • Our results also demonstrate how ETS1 and FLI-1 specifically regulate GADD153 expression [24].
  • However, the expression of the pro-apoptotic factor CHOP/GADD153 was induced and caspase-12 was activated in stressed aged rats but not in young animals [25].
  • We show that c-Myc represses the expression of GADD45a and GADD153 in response to thapsigargin, a nongenotoxic stress, as well as other endoplasmic reticulum (ER) stress agents. c-Myc represses both the basal expression and the magnitude of ER stress induction of GADD gene transcription [26].

Other interactions of DDIT3

  • In conclusion, Tf and other target genes identified may play a functional role in the downstream pathway of GADD153 [4].
  • These findings collectively indicated that activation of PPAR-gamma by TZDs could cause growth inhibition and apoptosis of NSCLC cells and that GADD153 might be a candidate factor implicated in these processes [17].
  • Activity of the GADD153 promoter occurred in a NSCLC cell line in transient transcription assays and was significantly stimulated by troglitazone, although binding of PPAR/retinoid X receptor heterodimer was not detected in the promoter region in gel retardation assays [17].
  • The expression of both GADD45 and GADD153 was increased in two cell lines following oil A treatment [27].
  • However, mRNA expression of GADD153 was increased most markedly in DOC-treated HCT-116 colonocytes, which express wild-type p53 [28].

Analytical, diagnostic and therapeutic context of DDIT3

  • In addition, the effect of DDIT3 and FUS-DDIT3 on the expression of other acute phase genes was examined using real-time PCR [2].
  • We screened 614 sequence-verified clones by Northern blotting, of which 42 genes were scored as over expressed and 17 genes as under expressed in GADD153 transfectants compared with control vector transfectants [4].
  • In the present study, we show that Fas receptor ligation or cellular treatment with synthetic C6-ceramide results in activation or phosphorylation, respectively, of the small G-protein Rac1, Jun N-terminal kinase (JNK)/p38 kinases (p38-K), and the transcription factor GADD153 [29].
  • Screening of a cDNA microarray chip containing 225 different genes revealed that GADD153 (growth arrest and DNA damage inducible gene), a transcription factor involved in apoptosis, showed the strongest differential expression following celecoxib treatment in all three cervical cancer cell lines [30].
  • GADD153 mRNA levels were measured in biopsies obtained before and 24 h after treatment with cDDP from 32 patients with stage III/IV head and neck cancer [31].


  1. Fusion of the FUS and BBF2H7 genes in low grade fibromyxoid sarcoma. Storlazzi, C.T., Mertens, F., Nascimento, A., Isaksson, M., Wejde, J., Brosjo, O., Mandahl, N., Panagopoulos, I. Hum. Mol. Genet. (2003) [Pubmed]
  2. Myxoid liposarcoma FUS-DDIT3 fusion oncogene induces C/EBP beta-mediated interleukin 6 expression. Göransson, M., Elias, E., Ståhlberg, A., Olofsson, A., Andersson, C., Aman, P. Int. J. Cancer (2005) [Pubmed]
  3. Expression of DOL54 is not restricted to myxoid liposarcomas with the FUS-DDIT3 chimera but is found in various sarcomas. Panagopoulos, I., Mertens, F., Isaksson, M., Mandahl, N. Oncol. Rep. (2004) [Pubmed]
  4. Transcriptional regulation of the human transferrin gene by GADD153 in hepatoma cells. You, K.R., Liu, M.J., Han, X.J., Lee, Z.W., Kim, D.G. Hepatology (2003) [Pubmed]
  5. Green tea polyphenol stimulates cancer preventive effects of celecoxib in human lung cancer cells by upregulation of GADD153 gene. Suganuma, M., Kurusu, M., Suzuki, K., Tasaki, E., Fujiki, H. Int. J. Cancer (2006) [Pubmed]
  6. A novel effector domain from the RNA-binding protein TLS or EWS is required for oncogenic transformation by CHOP. Zinszner, H., Albalat, R., Ron, D. Genes Dev. (1994) [Pubmed]
  7. CHOP (GADD153) and its oncogenic variant, TLS-CHOP, have opposing effects on the induction of G1/S arrest. Barone, M.V., Crozat, A., Tabaee, A., Philipson, L., Ron, D. Genes Dev. (1994) [Pubmed]
  8. A preoperative diagnostic test that distinguishes benign from malignant thyroid carcinoma based on gene expression. Cerutti, J.M., Delcelo, R., Amadei, M.J., Nakabashi, C., Maciel, R.M., Peterson, B., Shoemaker, J., Riggins, G.J. J. Clin. Invest. (2004) [Pubmed]
  9. Acetaldehyde impairs mitochondrial glutathione transport in HepG2 cells through endoplasmic reticulum stress. Lluis, J.M., Colell, A., García-Ruiz, C., Kaplowitz, N., Fernández-Checa, J.C. Gastroenterology (2003) [Pubmed]
  10. mda-7 (IL-24) Mediates selective apoptosis in human melanoma cells by inducing the coordinated overexpression of the GADD family of genes by means of p38 MAPK. Sarkar, D., Su, Z.Z., Lebedeva, I.V., Sauane, M., Gopalkrishnan, R.V., Valerie, K., Dent, P., Fisher, P.B. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  11. GADD153-mediated anticancer effects of N-(4-hydroxyphenyl)retinamide on human hepatoma cells. Kim, D.G., You, K.R., Liu, M.J., Choi, Y.K., Won, Y.S. J. Biol. Chem. (2002) [Pubmed]
  12. Physical and functional association between GADD153 and CCAAT/enhancer-binding protein beta during cellular stress. Fawcett, T.W., Eastman, H.B., Martindale, J.L., Holbrook, N.J. J. Biol. Chem. (1996) [Pubmed]
  13. Induction of GADD45 and GADD153 in neuroblastoma cells by dopamine-induced toxicity. Stokes, A.H., Freeman, W.M., Mitchell, S.G., Burnette, T.A., Hellmann, G.M., Vrana, K.E. Neurotoxicology (2002) [Pubmed]
  14. Repression of GADD153/CHOP by NF-kappaB: a possible cellular defense against endoplasmic reticulum stress-induced cell death. Nozaki, S., Sledge Jr, G.W., Nakshatri, H. Oncogene (2001) [Pubmed]
  15. Curcumin-induced GADD153 gene up-regulation in human colon cancer cells. Scott, D.W., Loo, G. Carcinogenesis (2004) [Pubmed]
  16. The Myxoid/Round Cell Liposarcoma Fusion Oncogene FUS-DDIT3 and the Normal DDIT3 Induce a Liposarcoma Phenotype in Transfected Human Fibrosarcoma Cells. Engström, K., Willén, H., Kåbjörn-Gustafsson, C., Andersson, C., Olsson, M., Göransson, M., Järnum, S., Olofsson, A., Warnhammar, E., Aman, P. Am. J. Pathol. (2006) [Pubmed]
  17. Activation of peroxisome proliferator-activated receptor-gamma stimulates the growth arrest and DNA-damage inducible 153 gene in non-small cell lung carcinoma cells. Satoh, T., Toyoda, M., Hoshino, H., Monden, T., Yamada, M., Shimizu, H., Miyamoto, K., Mori, M., Yamada, M., Mori, M. Oncogene (2002) [Pubmed]
  18. Expression and transactivating functions of the bZIP transcription factor GADD153 in mammary epithelial cells. Talukder, A.H., Wang, R.A., Kumar, R. Oncogene (2002) [Pubmed]
  19. Hydrogen peroxide induces GADD153 in Jurkat cells through the protein kinase C-dependent pathway. Oh-Hashi, K., Maehara, K., Isobe, K. Redox Rep. (2004) [Pubmed]
  20. Activator protein-1 and CCAAT/enhancer-binding protein mediated GADD153 expression is involved in deoxycholic acid-induced apoptosis. Qiao, D., Im, E., Qi, W., Martinez, J.D. Biochim. Biophys. Acta (2002) [Pubmed]
  21. Induction of a secreted protein by the myxoid liposarcoma oncogene. Kuroda, M., Wang, X., Sok, J., Yin, Y., Chung, P., Giannotti, J.W., Jacobs, K.A., Fitz, L.J., Murtha-Riel, P., Turner, K.J., Ron, D. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  22. C-reactive protein induces apoptosis in human coronary vascular smooth muscle cells. Blaschke, F., Bruemmer, D., Yin, F., Takata, Y., Wang, W., Fishbein, M.C., Okura, T., Higaki, J., Graf, K., Fleck, E., Hsueh, W.A., Law, R.E. Circulation (2004) [Pubmed]
  23. gadd153/Chop10, a potential target gene of the transcriptional repressor ATF3. Wolfgang, C.D., Chen, B.P., Martindale, J.L., Holbrook, N.J., Hai, T. Mol. Cell. Biol. (1997) [Pubmed]
  24. Regulation of the human stress response gene GADD153 expression: role of ETS1 and FLI-1 gene products. Seth, A., Giunta, S., Franceschil, C., Kola, I., Venanzoni, M.C. Cell Death Differ. (1999) [Pubmed]
  25. Cellular environment facilitates protein accumulation in aged rat hippocampus. Paz Gavilán, M., Vela, J., Castaño, A., Ramos, B., del Río, J.C., Vitorica, J., Ruano, D. Neurobiol. Aging (2006) [Pubmed]
  26. c-Myc represses the proximal promoters of GADD45a and GADD153 by a post-RNA polymerase II recruitment mechanism. Barsyte-Lovejoy, D., Mao, D.Y., Penn, L.Z. Oncogene (2004) [Pubmed]
  27. Oil A induces apoptosis of pancreatic cancer cells via caspase activation, redistribution of cell cycle and GADD expression. Dong, M.L., Zhu, Y.C., Hopkins, J.V. World J. Gastroenterol. (2003) [Pubmed]
  28. Increased GADD gene expression in human colon epithelial cells exposed to deoxycholate. Scott, D.W., Mutamba, S., Hopkins, R.G., Loo, G. J. Cell. Physiol. (2005) [Pubmed]
  29. Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153. Brenner, B., Koppenhoefer, U., Weinstock, C., Linderkamp, O., Lang, F., Gulbins, E. J. Biol. Chem. (1997) [Pubmed]
  30. GADD153 mediates celecoxib-induced apoptosis in cervical cancer cells. Kim, S.H., Hwang, C.I., Park, W.Y., Lee, J.H., Song, Y.S. Carcinogenesis (2006) [Pubmed]
  31. Quantitation of the change in GADD153 messenger RNA level as a molecular marker of tumor response in head and neck cancer. Los, G., Benbatoul, K., Gately, D.P., Barton, R., Christen, R., Robbins, K.T., Vicario, D., Kirmani, S., Orloff, L.A., Weisman, R., Howell, S.B. Clin. Cancer Res. (1999) [Pubmed]
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