ABSTRACT
@EN Many of the growth-promoting properties of growth hormone (GH) are mediated by insulin-like growth factor-I (IGF-I), a highly conserved circulation 70-amino acid peptide. Recent studies have shown that multiple mechanisms influence IGF-1 gene
expression, including transcription from two promoters, alternative RNA splicing and variable polyadenylation. In thyroid tissue, thyroid stimulating hormone (TSH) and TGF-I are the most possible candidates for follicular cell proliferation and
hypertrophy. Actually IGF-1 had autocrine and paracrine effect for tissue growing.
We prepared thyroid tumor tissue mRNAs using single step method for detecting IGF-I levels according to different tissues, i.e., thyroid adenoma or papillary thyroid carcinoma. We used Northern blot analysis for IGF-I mRNA and RNase protection
assay
(RPA) for IGF-I transcription start sites. For Northern blot, we used whole human IGF-I cDNA as a DNA probe and for RPA, we used IGF-I exon 1 containing noncoding promoter 1 as a riboprobe. We got good RNA bands from Northern blot analysis around
1
kb
(IGF-1A) and 7.5kb (IGF-1B) region. To clarify the amount of both IGF-1A and 1B mRNAs, we measured autoradinoraphied signal of IGF-1 mRNA's bands using densitometer. In IGR-1A signals, there's no change among liver and thyroid tissues, but in
case
of
IGF-1B mRNA bands, the signal was markedly increased in thyroid carcinoma tissues than that of normal thyroid tissue (85% vs 14%). In the study of RPA, all thyroid tissues used the same transcription start sites as those of liver's.
We concluded that that this different regulation of IGF-1 mRNA was originated from tissue specificity. That meant some tissue specific transcription factors were related to tissue IGF-1
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