Abstract:
:The IGF2 gene, which encodes a growth factor, is subject to genomic imprinting. The frequently observed loss of IGF2 imprinting in a variety of tumors has been suggested to contribute to neoplasia. Since these reports have not documented the imprinting status of IGF2 at the cellular level, it cannot be excluded that the imprinting status might vary within the tumor. The possibility that loss of IGF2 imprinting in neoplastic cells reflects random imprinting patterns, was therefore addressed. We show here that individual cell populations of the JEG-3 choriocarcinoma cell line display heterogenous imprinting patterns of both IGF2 and H19. In addition, a lack of correlation between IGF2 and H19 imprinting status suggests that any regional parental imprint has been functionally lost. This notion is reinforced by the observation that JEG-3 cell subclones display a range of promoter-specific IGF2 allele usage. Moreover, we observed that the imprinting status of H19 and IGF2 were differentially modulated in JEG-3-derived tumors generated in nude mice. The results suggest that allele-specific expression of IGF2 operates in the absence of a parental imprint. Finally, our observations urge caution with respect to the general interpretation of biallelic expression as 'loss of imprinting'.
journal_name
Oncogenejournal_title
Oncogeneauthors
He L,Cui H,Walsh C,Mattsson R,Lin W,Anneren G,Pfeifer-Ohlsson S,Ohlsson Rdoi
10.1038/sj.onc.1201501subject
Has Abstractpub_date
1998-01-08 00:00:00pages
113-9issue
1eissn
0950-9232issn
1476-5594journal_volume
16pub_type
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