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Int J Mol Med. 1998 Mar;1(3):617-20.

Alternative splicing of ERCC1 and cisplatin-DNA adduct repair in human tumor cell lines.

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1
Medical Ovarian Cancer Section, Developmental Therapeutics Department, 10/12N226, Medicine Branch, National Cancer Institute, Bethesda, MD 20892, USA.

Abstract

Alternative splicing is a common natural tool for the inhibition of function of full length gene products. We explored whether there was evidence that alternative splicing of ERCC1 may serve such a function for nucleotide excision repair. The ratio of alternatively spliced species to full length species was assessed for the protein and/or for the mRNA, for a series of human cell lines and tissues. This ratio was plotted against the amount of cisplatin-DNA adduct repair in each cell line (n=9), as measured by atomic absorbance spectrometry. As the percentage of alternatively spliced protein and/or mRNA increased, the amount of cisplatin-DNA adduct that was repaired was reduced. This inverse relationship was associated with a substantial amount of scatter (r=0.635), particularly at low levels of repair. These data demonstrate an association between alternative splicing of ERCC1, and reduction in cellular capability to repair cisplatin-DNA adduct.

PMID:
9852275
[Indexed for MEDLINE]
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