Adenovirus-mediated suppression of HMGI (Y) protein synthesis as potential therapy of human malignant neoplasias

S Scala, G Portella, M Fedele… - Proceedings of the …, 2000 - National Acad Sciences
Proceedings of the National Academy of Sciences, 2000National Acad Sciences
High mobility group I (HMGI) proteins are overexpressed in several human malignant
tumors. We previously demonstrated that inhibition of HMGI synthesis prevents thyroid cell
transformation. Here, we report that an adenovirus carrying the HMGI (Y) gene in an
antisense orientation (Ad-Yas) induced programmed cell death of two human thyroid
anaplastic carcinoma cell lines (ARO and FB-1), but not normal thyroid cells. The Ad-Yas
virus led to death of lung, colon, and breast carcinoma cells. A control adenovirus carrying …
High mobility group I (HMGI) proteins are overexpressed in several human malignant tumors. We previously demonstrated that inhibition of HMGI synthesis prevents thyroid cell transformation. Here, we report that an adenovirus carrying the HMGI(Y) gene in an antisense orientation (Ad-Yas) induced programmed cell death of two human thyroid anaplastic carcinoma cell lines (ARO and FB-1), but not normal thyroid cells. The Ad-Yas virus led to death of lung, colon, and breast carcinoma cells. A control adenovirus carrying the lacZ gene did not inhibit the growth of either normal or neoplastic cells. Ad-Yas treatment of tumors induced in athymic mice by ARO cells caused a drastic reduction in tumor size. Therefore, suppression of HMGI(Y) protein synthesis by an HMGI(Y) antisense adenoviral vector may be a useful treatment strategy in a variety of human malignant neoplasias, in which HMGI(Y) gene overexpression is a general event.
National Acad Sciences