Carcinogenesis, Vol. 20, No. 10, 2037,
October 1999
© 1999 Oxford University Press
Impairment of peroxisomal biogenesis in human colon carcinoma
The publishers wish to apologise for a series of errors which occurred in the above paper resulting in the incorrect identification of PPAR
as PPAR
in eight instances. The errors occur (i) in the Introduction (page 985), second paragraph, lines 5, 9, 11 and 13, (ii) in the Discussion (page 988), last paragraph, line 12 and (iii) in the References (page 989), reference numbers 24, 25 and 27. The correct paragraphs and references are reprinted below.
Introduction (second paragraph, 985)
The proliferation of peroxisomes and transcription of their genes is regulated by a subfamily of the ligand-activated nuclear hormone receptor superfamily, the so-called peroxisome proliferator activated receptor (PPAR) (23). Recent reports indicate that PPAR, a subtype of PPAR, plays a crucial role in the biology of colon cancer. Independent studies have revealed that the growth of several different colon carcinoma cell lines is inhibited by the ligand activation of PPAR (24) and that transplantable tumors in mice derived from human colon cancer cells show significant reduction of growth when mice are treated with troglitazone, a PPAR ligand (25). On the other hand, Lefebvre et al. (26) have reported that ligand activation of PPAR in C57BL/6J– APCMin/+ mice promotes the development of colon tumors, and Saez et al. (27) found that it accelerated the formation of colonic polyps in the same mice. Although the exact mechanism of those divergent observations remains to be elucidated, they all point to serious alterations of the peroxisomal compartment and its regulation in colon carcinoma.
Discussion (last paragraph, 988)
The mechanisms of the reduction of peroxisomes and their enzymes in colon carcinoma are not well understood. The results of the present study suggest that it could be due to a failure of the peroxisomal biogenesis rather than to a down-regulation of the specific genes for peroxisomal matrix proteins. The two important aspects of peroxisomal biogenesis, the synthesis of peroxisomal membranes, including the targeting of integral peroxisomal membrane proteins, and the matrix protein import, are mediated by quite distinct pathways (28,51,52). The question which of these mechanisms is impaired primarily in colon carcinoma cannot be answered as yet. However, since the ligand activation of PPAR by thiazolidinediones has been found to inhibit the growth of colon carcinoma (25), it would be tempting to speculate that such treatment would also lead to the recovery of the peroxisomes and their enzymes. Further analysis of this problem could lead to the elucidation of the role of peroxisomes in biology of the colon carcinoma.
Notes
by Christoph Lauer, Alfred Völkl, Stefan Riedl, H. Dariush Fahimi and Konstantin Beier
References
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Brockman,J.A., Gupta,R.A. and DuBois,R.N. (1998) Activation of PPAR leads to inhibition of anchorage-independent growth of human colorectal cancer cells. Gastroenterology, 115, 1049–1055.[Web of Science][Medline]
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Sarraf,P., Mueller,E., Jones,D., King,F.J., DeAngelo,D.J., Partridge,J.B., Holden,S.A., Chen,L.B., Singer,S., Fletcher,C. and Spiegelman,B.M. (1998) Differentiation and reversal of malignant changes in colon cancer through PPAR [see comments]. Nature Med., 4, 1046–1052.[Web of Science][Medline]
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Saez,E., Tontonoz,P., Nelson,M.C., Alvarez,J.G., Ming,U.T., Baird,S.M., Thomazy,V.A. and Evans,R.M. (1998) Activators of the nuclear receptor PPAR enhance colon polyp formation. Nature Med., 4, 1058–1061.[Web of Science][Medline]
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